Parkinson's disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. PD usually affects people over the age of 50.  Early symptoms of PD are subtle and occur gradually.  In some people the disease progresses more quickly than in others.   As the disease progresses, the shaking, or tremor, which affects the majority of PD patients may begin to interfere with daily activities.  Other symptoms may include depression and other emotional changes; difficulty in swallowing, chewing, and speaking; urinary problems or constipation; skin problems; and sleep disruptions.  There are currently no blood or laboratory tests that have been proven to help in diagnosing sporadic PD.  Therefore the diagnosis is based on medical history and a neurological examination.  The disease can be difficult to diagnose accurately.   Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. Parkinson's disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. PD usually affects people over the age of 50.  Early symptoms of PD are subtle and occur gradually.  In some people the disease progresses more quickly than in others.   As the disease progresses, the shaking, or tremor, which affects the majority of PD patients may begin to interfere with daily activities.  Other symptoms may include depression and other emotional changes; difficulty in swallowing, chewing, and speaking; urinary problems or constipation; skin problems; and sleep disruptions.  There are currently no blood or laboratory tests that have been proven to help in diagnosing sporadic PD.  Therefore the diagnosis is based on medical history and a neurological examination.  The disease can be difficult to diagnose accurately.   Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. Parkinson's disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of do

1. Fitango Education
Health Topics
Parkinson's
http://www.fitango.com/categories.php?id=272

2. Overview
Parkinson's disease (PD) belongs to a group
of conditions called motor system disorders, which
are the result of the loss
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
1

3. Overview
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
limbs and trunk; bradykinesia, or slowness of
movement; and postural
instability, or impaired balance and coordination.
As these symptoms become
2

4. Overview
more pronounced, patients may have difficulty
walking, talking, or completing
other simple tasks. PD usually affects people over
the age of 50.  Early
symptoms of PD are subtle and occur
gradually.  In some people the disease
3

5. Overview
progresses more quickly than in
others.  
As the disease progresses, the
shaking, or tremor, which affects the majority of
PD patients may begin to
interfere with daily activities.  Other
symptoms may include depression
4

6. Overview
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
urinary problems or constipation; skin problems;
and sleep disruptions. 
There are currently no blood or laboratory tests
that have been proven to help
5

7. Overview
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
history and a neurological examination.  The
disease can be difficult to
diagnose accurately.   Doctors may
sometimes request brain scans or
6

8. Overview
laboratory tests in order to rule out other diseases.
Parkinson's disease (PD) belongs to a group
of conditions called motor system disorders, which
are the result of the loss
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
7

9. Overview
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
limbs and trunk; bradykinesia, or slowness of
movement; and postural
instability, or impaired balance and coordination.
As these symptoms become
8

10. Overview
more pronounced, patients may have difficulty
walking, talking, or completing
other simple tasks. PD usually affects people over
the age of 50.  Early
symptoms of PD are subtle and occur
gradually.  In some people the disease
9

11. Overview
progresses more quickly than in others.  
As the disease progresses, the
shaking, or tremor, which affects the majority of
PD patients may begin to
interfere with daily activities.  Other
symptoms may include depression
10

12. Overview
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
urinary problems or constipation; skin problems;
and sleep disruptions. 
There are currently no blood or laboratory tests
that have been proven to help
11

13. Overview
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
history and a neurological examination.  The
disease can be difficult to
diagnose accurately.   Doctors may
sometimes request brain scans or
12

14. Overview
laboratory tests in order to rule out other diseases.
Parkinson's disease (PD) belongs to a group
of conditions called motor system disorders, which
are the result of the loss
13

15. Overview
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
limbs and trunk; bradykinesia, or slowness of
movement; and postural
14

16. Overview
instability, or impaired balance and coordination.
As these symptoms become
more pronounced, patients may have difficulty
walking, talking, or completing
other simple tasks. PD usually affects people over
the age of 50.  Early
15

17. Overview
symptoms of PD are subtle and occur
gradually.  In some people the disease
progresses more quickly than in
others.  
As the disease progresses, the
shaking, or tremor, which affects the majority of
PD patients may begin to
16

18. Overview
interfere with daily activities.  Other
symptoms may include depression
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
urinary problems or constipation; skin problems;
and sleep disruptions. 
17

19. Overview
There are currently no blood or laboratory tests
that have been proven to help
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
history and a neurological examination.  The
disease can be difficult to
18

20. Overview
diagnose accurately.   Doctors may
sometimes request brain scans or
laboratory tests in order to rule out other diseases.
Parkinson's disease (PD) belongs to a group
of conditions called motor system disorders, which
are the result of the loss
19

21. Overview
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
limbs and trunk; bradykinesia, or slowness of
movement; and postural
20

22. Overview
instability, or impaired balance and coordination.
As these symptoms become
more pronounced, patients may have difficulty
walking, talking, or completing
other simple tasks. PD usually affects people over
the age of 50.  Early
21

23. Overview
symptoms of PD are subtle and occur
gradually.  In some people the disease
progresses more quickly than in others.  
As the disease progresses, the
shaking, or tremor, which affects the majority of
PD patients may begin to
22

24. Overview
interfere with daily activities.  Other
symptoms may include depression
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
urinary problems or constipation; skin problems;
and sleep disruptions. 
23

25. Overview
There are currently no blood or laboratory tests
that have been proven to help
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
history and a neurological examination.  The
disease can be difficult to
24

26. Overview
diagnose accurately.   Doctors may
sometimes request brain scans or
laboratory tests in order to rule out other diseases.
Parkinson's disease (PD) belongs to a group
25

27. Overview
of conditions called motor system disorders, which
are the result of the loss
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
26

28. Overview
limbs and trunk; bradykinesia, or slowness of
movement; and postural
instability, or impaired balance and coordination.
As these symptoms become
more pronounced, patients may have difficulty
walking, talking, or completing
27

29. Overview
other simple tasks. PD usually affects people over
the age of 50.  Early
symptoms of PD are subtle and occur
gradually.  In some people the disease
progresses more quickly than in
others.  
As the disease progresses, the
28

30. Overview
shaking, or tremor, which affects the majority of
PD patients may begin to
interfere with daily activities.  Other
symptoms may include depression
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
29

31. Overview
urinary problems or constipation; skin problems;
and sleep disruptions. 
There are currently no blood or laboratory tests
that have been proven to help
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
30

32. Overview
history and a neurological examination.  The
disease can be difficult to
diagnose accurately.   Doctors may
sometimes request brain scans or
laboratory tests in order to rule out other diseases.
Parkinson's disease (PD) belongs to a group
31

33. Overview
of conditions called motor system disorders, which
are the result of the loss
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
32

34. Overview
limbs and trunk; bradykinesia, or slowness of
movement; and postural
instability, or impaired balance and coordination.
As these symptoms become
more pronounced, patients may have difficulty
walking, talking, or completing
33

35. Overview
other simple tasks. PD usually affects people over
the age of 50.  Early
symptoms of PD are subtle and occur
gradually.  In some people the disease
progresses more quickly than in others.  
As the disease progresses, the
34

36. Overview
shaking, or tremor, which affects the majority of
PD patients may begin to
interfere with daily activities.  Other
symptoms may include depression
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
35

37. Overview
urinary problems or constipation; skin problems;
and sleep disruptions. 
There are currently no blood or laboratory tests
that have been proven to help
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
36

38. Overview
history and a neurological examination.  The
disease can be difficult to
diagnose accurately.   Doctors may
sometimes request brain scans or
laboratory tests in order to rule out other diseases.
37

39. Overview
Parkinson's disease (PD) belongs to a group
of conditions called motor system disorders, which
are the result of the loss
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
38

40. Overview
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
limbs and trunk; bradykinesia, or slowness of
movement; and postural
instability, or impaired balance and coordination.
As these symptoms become
39

41. Overview
more pronounced, patients may have difficulty
walking, talking, or completing
other simple tasks. PD usually affects people over
the age of 50.  Early
symptoms of PD are subtle and occur
gradually.  In some people the disease
40

42. Overview
progresses more quickly than in
others.  
As the disease progresses, the
shaking, or tremor, which affects the majority of
PD patients may begin to
interfere with daily activities.  Other
symptoms may include depression
41

43. Overview
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
urinary problems or constipation; skin problems;
and sleep disruptions. 
There are currently no blood or laboratory tests
that have been proven to help
42

44. Overview
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
history and a neurological examination.  The
disease can be difficult to
diagnose accurately.   Doctors may
sometimes request brain scans or
43

45. Overview
laboratory tests in order to rule out other diseases.
Parkinson's disease (PD) belongs to a group
of conditions called motor system disorders, which
are the result of the loss
of dopamine-producing brain cells. The four
primary symptoms of PD are tremor,
44

46. Overview
or trembling in hands, arms, legs, jaw, and face;
rigidity, or stiffness of the
limbs and trunk; bradykinesia, or slowness of
movement; and postural
instability, or impaired balance and coordination.
As these symptoms become
45

47. Overview
more pronounced, patients may have difficulty
walking, talking, or completing
other simple tasks. PD usually affects people over
the age of 50.  Early
symptoms of PD are subtle and occur
gradually.  In some people the disease
46

48. Overview
progresses more quickly than in others.  
As the disease progresses, the
shaking, or tremor, which affects the majority of
PD patients may begin to
interfere with daily activities.  Other
symptoms may include depression
47

49. Overview
and other emotional changes; difficulty in
swallowing, chewing, and speaking;
urinary problems or constipation; skin problems;
and sleep disruptions. 
There are currently no blood or laboratory tests
that have been proven to help
48

50. Overview
in diagnosing sporadic PD.  Therefore the
diagnosis is based on medical
history and a neurological examination.  The
disease can be difficult to
diagnose accurately.   Doctors may
sometimes request brain scans or
49

51. Overview
laboratory tests in order to rule out other diseases.
50

52. Symptoms
Early symptoms of PD are subtle and occur
gradually. Affected people may feel mild tremors
or have difficulty getting out
of a chair.  They may notice that they speak
too softly or that their
51

53. Symptoms
handwriting is slow and looks cramped or small.
They may lose track of a word
or thought, or they may feel tired, irritable, or
depressed for no apparent
reason. This very early period may last a long time
before the more classic and
obvious symptoms appear. 52

54. Symptoms
Friends or family members may be the first
to notice changes in someone with early PD. They
may see that the person's face
53

55. Symptoms
person does not move an arm or leg normally.
They also may notice that the
person seems stiff, unsteady, or unusually slow.
As the disease progresses, the shaking or 54

56. Symptoms
tremor that affects the majority of Parkinson's
patients may begin to interfere
with daily activities. Patients may not be able to
hold utensils steady or they
may find that the shaking makes reading a
newspaper difficult. Tremor is
55

57. Symptoms
usually the symptom that causes people to seek
medical help.
People with PD often develop a so-
called parkinsonian
56

58. Symptoms
hurrying forward (called festination), and reduced
swinging of the arms. They
also may have trouble initiating movement (start
hesitation), and they may stop
suddenly as they walk (freezing).
57

59. Symptoms
PD does not affect everyone the same way,
and the rate of progression differs among
patients.  Tremor is the major
symptom for some patients, while for
others, tremor is nonexistent or very
minor.
58

60. Symptoms
PD symptoms often begin on one side of the
body.  However, as it progresses, the disease
eventually affects
59

61. Symptoms
symptoms are often less severe on one side than
on the other.  The four
primary symptoms of PD are:
-- **Tremor** 60

62. Symptoms
. The tremor associated with PD has a
characteristic appearance. Typically, the tremor
takes the form of a rhythmic
back-and-forth motion at a rate of 4-6 beats per
second. It may involve the
thumb and forefinger and appear as a "pill rolling"
tremor.  61

63. Symptoms
Tremor often begins in a hand, although
sometimes a foot or the jaw is affected
first. It is most obvious when the hand is at rest or
when a person is under
stress.  For example, the shaking may
become more pronounced a few seconds
62

64. Symptoms
after the hands are rested on a table. 
Tremor usually disappears during
sleep or improves with intentional movement.
-- **Rigidity**
. Rigidity, or a resistance to
63

65. Symptoms
movement, affects most people with PD. A major
principle of body movement is
that all muscles have an opposing muscle.
Movement is possible not just because
one muscle becomes more active, but because the
opposing muscle relaxes. In PD,
64

66. Symptoms
rigidity comes about when, in response to signals
from the brain, the delicate
balance of opposing muscles is disturbed. The
muscles remain constantly tensed
and contracted so that the person aches or feels
stiff or weak. The rigidity
65

67. Symptoms
becomes obvious when another person tries to
move the patient's arm, which will
move only in ratchet-like or short, jerky
movements known as
"cogwheel" rigidity.
-- **Bradykinesia**
66

68. Symptoms
. Bradykinesia, or the slowing
down and loss of spontaneous and automatic
movement, is particularly
frustrating because it may make simple tasks
somewhat difficult.  The
person cannot rapidly perform routine
movements. Activities once performed 67

69. Symptoms
quickly and easily — such as washing or dressing
— may take several hours.
-- **Postural instability**
. Postural instability,
or impaired balance, causes patients to fall
easily.  Affected people also
68

70. Symptoms
may develop a stooped posture in which the head
is bowed and the shoulders are
drooped. 
69

71. Symptoms
Early symptoms of PD are subtle and occur
gradually. Affected people may feel mild tremors
or have difficulty getting out
of a chair.  They may notice that they speak
too softly or that their
handwriting is slow and looks cramped or small.
They may lose track of a word 70

72. Symptoms
or thought, or they may feel tired, irritable, or
depressed for no apparent
reason. This very early period may last a long time
before the more classic and
obvious symptoms appear.
71

73. Symptoms
Friends or family members may be the first
to notice changes in someone with early PD. They
may see that the person's face
lacks expression and animation (known as "masked
face") or that the
person does not move an arm or leg normally.
They also may notice that the 72

74. Symptoms
person seems stiff, unsteady, or unusually slow.
As the disease progresses, the shaking or
tremor that affects the majority of Parkinson's
patients may begin to interfere 73

75. Symptoms
with daily activities. Patients may not be able to
hold utensils steady or they
may find that the shaking makes reading a
newspaper difficult. Tremor is
usually the symptom that causes people to seek
medical help.
74

76. Symptoms
People with PD often develop a so-
called parkinsonian
gait that includes a tendency to lean
forward, small quick steps as if
hurrying forward (called festination), and reduced
swinging of the arms. They 75

77. Symptoms
also may have trouble initiating movement (start
hesitation), and they may stop
suddenly as they walk (freezing).
PD does not affect everyone the same way, 76

78. Symptoms
and the rate of progression differs among
patients.  Tremor is the major
symptom for some patients, while for
others, tremor is nonexistent or very
minor.
77

79. Symptoms
PD symptoms often begin on one side of the
body.  However, as it progresses, the disease
eventually affects
both sides.  Even after the disease involves
both sides of the body, the
symptoms are often less severe on one side than
on the other.  The four 78

80. Symptoms
primary symptoms of PD are:
-- **Tremor**
. The tremor associated with PD has a
79

81. Symptoms
characteristic appearance. Typically, the tremor
takes the form of a rhythmic
back-and-forth motion at a rate of 4-6 beats per
second. It may involve the
thumb and forefinger and appear as a "pill rolling"
tremor. 
80

82. Symptoms
Tremor often begins in a hand, although
sometimes a foot or the jaw is affected
first. It is most obvious when the hand is at rest or
when a person is under
stress.  For example, the shaking may
become more pronounced a few seconds
81

83. Symptoms
after the hands are rested on a table. 
Tremor usually disappears during
sleep or improves with intentional movement.
-- **Rigidity**
. Rigidity, or a resistance to
82

84. Symptoms
movement, affects most people with PD. A major
principle of body movement is
that all muscles have an opposing muscle.
Movement is possible not just because
one muscle becomes more active, but because the
opposing muscle relaxes. In PD,
83

85. Symptoms
rigidity comes about when, in response to signals
from the brain, the delicate
balance of opposing muscles is disturbed. The
muscles remain constantly tensed
and contracted so that the person aches or feels
stiff or weak. The rigidity
84

86. Symptoms
becomes obvious when another person tries to
move the patient's arm, which will
move only in ratchet-like or short, jerky
movements known as
"cogwheel" rigidity.
-- **Bradykinesia**
85

87. Symptoms
. Bradykinesia, or the slowing
down and loss of spontaneous and automatic
movement, is particularly
frustrating because it may make simple tasks
somewhat difficult.  The
person cannot rapidly perform routine
movements. Activities once performed 86

88. Symptoms
quickly and easily — such as washing or dressing
— may take several hours.
-- **Postural instability**
. Postural instability,
or impaired balance, causes patients to fall
easily.  Affected people also
87

89. Symptoms
may develop a stooped posture in which the head
is bowed and the shoulders are
drooped. 
88

90. Treatment
At present, there is no cure for PD, but a variety of
medications provide dramatic relief from the
symptoms. Usually, patients are given levodopa
combined with carbidopa. Carbidopa delays the
conversion of levodopa into dopamine until it
reaches the brain.
89

91. Treatment
Nerve cells can use levodopa to make dopamine
and replenish the brain's dwindling supply.
Although levodopa helps at least three-quarters of
parkinsonian cases, not all symptoms respond
equally to the drug. Bradykinesia and rigidity
respond best, while tremor may be only marginally
reduced. Problems with balance and other
symptoms may not be alleviated at all.
Anticholinergics may help control tremor and
rigidity. 
90

92. Treatment
Other drugs, such as
bromocriptine, pramipexole, and ropinirole, mimic
the role of dopamine in the brain, causing the
neurons to react as they would to dopamine. An
antiviral drug, amantadine, also appears to reduce
symptoms. In May 2006, the FDA approved
rasagiline to be used along with levodopa for
patients with advanced PD or as a single-drug
treatment for early PD. 
91

93. Treatment
In some cases, surgery may be appropriate if the
disease doesn't respond to drugs. A therapy called
deep brain stimulation (DBS) has now been
approved by the U.S. Food and Drug
Administration. In DBS, electrodes are implanted
into the brain and connected to a small electrical
device called a pulse generator that can be
externally programmed. 
92

94. Treatment
DBS can reduce the need for levodopa and related
drugs, which in turn decreases the involuntary
movements called dyskinesias that are a common
side effect of levodopa. It also helps to alleviate
fluctuations of symptoms and to reduce
tremors, slowness of movements, and gait
problems. DBS requires careful programming of
the stimulator device in order to work correctly.
93

95. Treatment
At present, there is no cure for PD, but a variety of
medications provide dramatic relief from the
symptoms. Usually, patients are given levodopa
combined with carbidopa. Carbidopa delays the
conversion of levodopa into dopamine until it
reaches the brain.
94

96. Treatment
Nerve cells can use levodopa to make dopamine
and replenish the brain's dwindling supply.
Although levodopa helps at least three-quarters of
parkinsonian cases, not all symptoms respond
equally to the drug. Bradykinesia and rigidity
respond best, while tremor may be only marginally
reduced. Problems with balance and other
symptoms may not be alleviated at all.
Anticholinergics may help control tremor and
rigidity. 
95

97. Treatment
Other drugs, such as bromocriptine, pramipexole,
and ropinirole, mimic the role of dopamine in the
brain, causing the neurons to react as they would
to dopamine. An antiviral drug, amantadine, also
appears to reduce symptoms. In May 2006, the
FDA approved rasagiline to be used along with
levodopa for patients with advanced PD or as a
single-drug treatment for early PD. 
96

98. Treatment
In some cases, surgery may be appropriate if the
disease doesn't respond to drugs. A therapy called
deep brain stimulation (DBS) has now been
approved by the U.S. Food and Drug
Administration. In DBS, electrodes are implanted
into the brain and connected to a small electrical
device called a pulse generator that can be
externally programmed. 
97

99. Treatment
DBS can reduce the need for levodopa and related
drugs, which in turn decreases the involuntary
movements called dyskinesias that are a common
side effect of levodopa. It also helps to alleviate
fluctuations of symptoms and to reduce tremors,
slowness of movements, and gait problems. DBS
requires careful programming of the stimulator
device in order to work correctly.
98

100. Prognosis
PD is not by itself a fatal disease, but it
does get worse with time.   The average life
expectancy of a PD patient is
generally the same as for people who do not have
the disease.  However, in
99

101. Prognosis
the late stages of the disease, PD may cause
complications such as choking,
pneumonia, and falls that can lead to
death.  Fortunately, there are many
treatment options available for people with PD.
100

102. Prognosis
The progression of symptoms in PD may take
20 years or more.  In some
people, however, the disease progresses more
quickly.  There is no way to predict what
course the disease will take for
101

103. Prognosis
an individual person.  One commonly used
system for describing how the
symptoms of PD progress is called the Hoehn and
Yahr scale.
102

104. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Disease**
103

105. Prognosis
**Hoehn and Yahr Staging of Parkinson's
**Stage one**
Symptoms on one side of the body only.
104

106. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Symptoms on both sides of the body. 
No impairment of balance.
**Stage three**
105

107. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Balance impairment.  Mild to
moderate disease.  Physically independent.
**Stage four**
106

108. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Severe disability, but still able to walk
or stand unassisted.
**Stage five**
107

109. Prognosis
**Hoehn and Yahr Staging of Parkinson's
assisted.
108

110. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Another commonly used scale is the Unified
Parkinson's Disease Rating Scale (UPDRS). This
much more complicated scale has
multiple ratings that measure mental
functioning, behavior, and mood;
activities of daily living; and motor function. Both
the Hoehn and Yahr scale 109

111. Prognosis
**Hoehn and Yahr Staging of Parkinson's
and the UPDRS are used to measure how
individuals are faring and how much
treatments are helping them.
With appropriate treatment, most people 110

112. Prognosis
**Hoehn and Yahr Staging of Parkinson's
with PD can live productive lives for many years
after diagnosis. 
PD is not by itself a fatal disease, but it
does get worse with time.   The average life
expectancy of a PD patient is
generally the same as for people who do not have
the disease.  However, in
111

113. Prognosis
**Hoehn and Yahr Staging of Parkinson's
the late stages of the disease, PD may cause
complications such as choking,
pneumonia, and falls that can lead to
death.  Fortunately, there are many
treatment options available for people with PD.
112

114. Prognosis
**Hoehn and Yahr Staging of Parkinson's
The progression of symptoms in PD may take
20 years or more.  In some
people, however, the disease progresses more
quickly.  There is no way to predict what
course the disease will take for
113

115. Prognosis
**Hoehn and Yahr Staging of Parkinson's
an individual person.  One commonly used
system for describing how the
symptoms of PD progress is called the Hoehn and
Yahr scale.
114

116. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Disease**
115

117. Prognosis
**Hoehn and Yahr Staging of Parkinson's
**Stage one**
Symptoms on one side of the body only.
116

118. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Symptoms on both sides of the body. 
No impairment of balance.
**Stage three**
117

119. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Balance impairment.  Mild to
moderate disease.  Physically independent.
**Stage four**
118

120. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Severe disability, but still able to walk
or stand unassisted.
**Stage five**
119

121. Prognosis
**Hoehn and Yahr Staging of Parkinson's
assisted.
120

122. Prognosis
**Hoehn and Yahr Staging of Parkinson's
Another commonly used scale is the Unified
Parkinson's Disease Rating Scale (UPDRS). This
much more complicated scale has
multiple ratings that measure mental
functioning, behavior, and mood;
activities of daily living; and motor function. Both
the Hoehn and Yahr scale 121

123. Prognosis
**Hoehn and Yahr Staging of Parkinson's
and the UPDRS are used to measure how
individuals are faring and how much
treatments are helping them.
With appropriate treatment, most people 122

124. Prognosis
**Hoehn and Yahr Staging of Parkinson's
with PD can live productive lives for many years
after diagnosis. 
123

125. Research
In recent years, Parkinson's research has
advanced to the point that halting the progression
of PD, restoring lost
function, and even preventing the disease are all
considered realistic
124

126. Research
goals.  While the ultimate goal of preventing
PD may take years to achieve,
researchers are making great progress in
understanding and treating PD.
125

127. Research
research is genetics.  Studying the genes
responsible for inherited cases
can help researchers understand both inherited
and sporadic cases of the disease.
Identifying gene defects can also help researchers
understand how PD occurs,
126

128. Research
develop animal models that accurately mimic the
neuronal death in human PD,
identify new drug targets, and improve diagnosis.
As discussed in the “What Genes are Linked 127

129. Research
to Parkinson's Disease?" section, several genes
have been definitively
linked to PD in some people.  Researchers
also have identified a number of
other genes that may play a role and are working
to confirm these
128

130. Research
findings.  In addition, several chromosomal
regions have been linked to PD
in some families.  Researchers hope to
identify the genes located in these
chromosomal regions and to determine which of
them may play roles in PD.
129

131. Research
Researchers funded by NINDS are gathering
information and DNA samples from hundreds of
families with PD and are
conducting large-scale gene expression studies to
identify genes that are
130

132. Research
abnormally active or inactive in PD.  They
also are comparing gene
activity in PD with gene activity in similar diseases
such as progressive supranuclear
palsy. 
131

133. Research
Some scientists have found evidence that
specific variations in the DNA of mitochondria –
structures in cells that
provide the energy for cellular activity — can
increase the risk of getting PD,
132

134. Research
while other variations are associated with a
lowered risk of the disorder. They
also have found that PD patients have more
mitochondrial DNA (mtDNA) variations
than patients with other movement disorders or
Alzheimer's disease. Researchers
133

135. Research
are working to define how these mtDNA variations
may lead to PD.
In addition to identifying new genes for
PD, researchers are trying to learn how known PD 134

136. Research
gene mutations cause disease.  For
example, a 2005 study found that the
normal alpha-synuclein protein may help other
proteins that are important for
nerve transmission to fold correctly.  Other
studies have suggested that
135

137. Research
the normal parkin protein protects neurons from a
variety of threats, including
alpha-synuclein toxicity and excitotoxicity.
Scientists continue to study environmental 136

138. Research
toxins such as pesticides and herbicides that can
cause PD symptoms in
animals.  They have found that exposing
rodents to the pesticide rotenone
and several other agricultural chemicals can cause
cellular and behavioral
137

139. Research
changes that mimic those seen in PD.  Other
studies have suggested that
prenatal exposure to certain toxins can increase
susceptibility to PD in
adulthood. An NIH-sponsored program
called the Collaborative Centers
138

140. Research
for Parkinson's Disease Environmental Research
(CCPDER) focuses on how
occupational exposure to toxins and use of caffeine
and other substances may
affect the risk of PD.
139

141. Research
Another major area of PD research involves
the cell's protein disposal system, called the
ubiquitin-proteasome system. If
this disposal system fails to work correctly, toxins
and other substances may
build up to harmful levels, leading to cell
death.  The 140

142. Research
ubiquitin-proteasome system requires interactions
between several proteins,
including parkin and UCH-L1. Therefore, disruption
of the ubiquitin-proteasome
system may partially explain how mutations in
these genes cause PD.
141

143. Research
Other studies focus on how Lewy bodies form
and what role they play in PD.  Some studies
suggest that Lewy bodies are
a byproduct of degenerative processes within
neurons, while others indicate
142

144. Research
that Lewy bodies are a protective mechanism by
which neurons lock away abnormal
molecules that might otherwise be harmful. 
Additional studies have found
that alpha-synuclein clumps alter gene expression
and bind to vesicles within
143

145. Research
the cell in ways that could be harmful. 
Another common topic of PD research is
excitotoxicity – overstimulation of nerve cells that
leads to cell damage or 144

146. Research
death. In excitotoxicity, the brain becomes
oversensitized to the
neurotransmitter glutamate, which increases
activity in the brain. The dopamine
deficiency in PD causes overactivity of neurons in
the subthalamic nucleus,
145

147. Research
which may lead to excitotoxic damage there and in
other parts of the brain.
Researchers also have found that dysfunction of
the cells' mitochondria can
make dopamine-producing neurons vulnerable to
glutamate. 
146

148. Research
Other researchers are focusing on how
inflammation may affect PD. Inflammation is
common to a variety of
neurodegenerative diseases, including
PD, Alzheimer's disease, HIV-1-associated
147

149. Research
dementia, and amyotrophic lateral sclerosis.
Several studies have shown that
inflammation-promoting molecules increase cell
death after treatment with the
toxin MPTP. Inhibiting the inflammation with drugs
or by genetic engineering
148

150. Research
prevented some of the neuronal degeneration in
these studies.  Other
research has shown that dopamine neurons in
brains from patients with PD have
higher levels of an inflammatory enzyme called
COX-2 than those of people
149

151. Research
without PD.  Inhibiting COX-2 doubled the
number of neurons that survived
in a mouse model for PD.
Since the discovery that MPTP causes 150

152. Research
parkinsonian symptoms in humans, scientists have
found that by injecting MPTP
and certain other toxins into laboratory
animals, they can reproduce the brain
lesions that cause these symptoms. This allows
them to study the mechanisms of
151

153. Research
the disease and helps in the development of new
treatments.  They also
have developed animal models with alterations of
the alpha-synuclein and parkin
genes.  Other researchers have used genetic
engineering to develop mice
152

154. Research
with disrupted mitochondrial function in dopamine
neurons.  These animals
have many of the characteristics associated with
PD.
153

155. Research
characteristics that can reveal whether the disease
is developing or
progressing – are another focus of research. 
Such biomarkers could help
doctors detect the disease before symptoms
appear and improve diagnosis of the
154

156. Research
disease.  They also would show if
medications and other types of therapy
have a positive or negative effect on the course of
the disease.  Some of
the most promising biomarkers for PD are brain
imaging techniques.  For
155

157. Research
example, some researchers are using positron
emission tomography (PET) brain
scans to try to identify metabolic changes in the
brains of people with PD and
to determine how these changes relate to disease
symptoms.  Other
156

158. Research
potential biomarkers for PD include alterations in
gene expression.
Researchers also are conducting many
studies of new or improved therapies for 157

159. Research
(DBS) is now FDA-approved and has been used in
thousands of people with PD,
researchers continue to try to improve the
technology and surgical techniques
in this therapy.  For example, some studies
are comparing DBS to the best
158

160. Research
medical therapy and trying to determine which
part of the brain is the best
location for stimulation.  Another clinical
trial is studying how DBS
affects depression and quality of life. 
159

161. Research
Other clinical studies are testing whether
transcranial electrical polarization (TEP) or
transcranial magnetic stimulation
(TMS) can reduce the symptoms of PD. In
TEP, electrodes placed on the scalp are
160

162. Research
used to generate an electrical current that
modifies signals in the brain's
cortex.  In TMS, an insulated coil of wire on
the scalp is used to
generate a brief electrical current.
161

163. Research
One of the enduring questions in PD
research has been how treatment with levodopa
and other dopaminergic drugs
affects progression of the disease. 
Researchers are continuing to try to
clarify these effects.  One study has
suggested that PD patients with a 162

164. Research
low-activity variant of the gene for COMT (which
breaks down dopamine) perform
worse than others on tests of cognition, and that
dopaminergic drugs may worsen
cognition in these people, perhaps because the
reduced COMT activity causes
163

165. Research
dopamine to build up to harmful levels in some
parts of the brain.  In the
future, it may become possible to test for such
individual gene differences in
order to improve treatment of PD.
164

166. Research
A variety of new drug treatments are in
clinical trials for PD.  These include a drug
called GM1 ganglioside that
increases dopamine levels in the brain. 
Researchers are testing whether
165

167. Research
this drug can reduce symptoms, delay disease
progression, or partially restore
damaged brain cells in PD patients.  Other
studies are testing whether a
drug called istradefylline can improve motor
function in PD, and whether a drug
166

168. Research
called ACP-103 that blocks receptors for the
neurotransmitter serotonin will
lessen the severity of parkinsonian symptoms and
levodopa-associated
complications in PD patients. Other topics of
research include
167

169. Research
controlled-release formulas of PD drugs and
implantable pumps that give a
continuous supply of levodopa.
Some researchers are testing potential 168

170. Research
neuroprotective drugs to see if they can slow the
progression of PD.  One
study, called NET-PD (Neuroexploratory Trials in
Parkinson's Disease), is
evaluating minocycline, creatine, coenzyme Q10,
and GPI-1485 to determine if
169

171. Research
any of these agents should be considered for
further testing.  The NET-PD
study may evaluate other possible neuroprotective
agents in the future. 
Drugs found to be successful in the pilot phases
may move to large phase III
170

172. Research
trials involving hundreds of patients.  A
separate group of researchers is
investigating the effects of either 1200 or 2400
milligrams of coenzyme Q10 in
600 patients.   Several MAO-B inhibitors,
including selegiline,
171

173. Research
lazabemide, and rasagiline, also are in clinical trials
to determine if they
have neuroprotective effects in people with PD.
Nerve growth factors, or neurotrophic 172

174. Research
factors, which support survival, growth, and
development of brain cells, are
another type of potential therapy for PD. 
One such drug, glial cell
line-derived neurotrophic factor (GDNF), has been
shown to protect dopamine
173

175. Research
neurons and to promote their survival in animal
models of PD.  This drug
has been tested in several clinical trials for people
with PD, and the drug
appeared to cause regrowth of dopamine nerve
fibers in one person who received
174

176. Research
the drug.  However, a phase II clinical study
of GDNF was halted in 2004
because the treatment did not show any clinical
benefit after 6 months, and
some data suggested that it might even be
harmful.  Other neurotrophins
175

177. Research
that may be useful for treating PD include
neurotrophin-4 (NT-4), brain-derived
neurotrophic factor (BDNF), and fibroblast growth
factor 2 (FGF-2).
176

178. Research
dietary supplements can slow PD, several clinical
studies are testing whether
supplementation with vitamin B12 and other
substances may be helpful. A 2005
study found that dietary restriction — reducing the
number of calories normally
177

179. Research
consumed – helped to increase abnormally low
levels of the neurotransmitter
glutamate in a mouse model for early PD. 
The study also suggested that
dietary restriction affected dopamine activity in
the brain.  Another
178

180. Research
study showed that dietary restriction before the
onset of PD in a mouse model
helped to protect dopamine-producing
neurons. 
179

181. Research
that might improve some of the secondary
symptoms of PD, such as depression and
swallowing disorders.  One clinical trial is
investigating whether a drug
called quetiapine can reduce psychosis or agitation
in PD patients with
180

182. Research
dementia and in dementia patients with
parkinsonian symptoms. Some studies also
are examining whether transcranial magnetic
stimulation or a food supplement
called s-adenosyl-methionine (SAM-e) can alleviate
depression in people with
181

183. Research
PD, and whether levetiracetam, a drug approved to
treat epilepsy, can reduce
dyskinesias in Parkinson's patients without
interfering with other PD drugs.
182

184. Research
implant cells to replace those lost in the
disease.  Researchers are
conducting clinical trials of a cell therapy in which
human retinal epithelial
cells attached to microscopic gelatin beads are
implanted into the brains of
183

185. Research
people with advanced PD.  The retinal
epithelial cells produce
levodopa.  The investigators hope that this
therapy will enhance brain
levels of dopamine.
184

186. Research
Starting in the 1990s, researchers
conducted a controlled clinical trial of fetal tissue
implants in
people with PD. They attempted to replace
lost dopamine-producing neurons
with healthy ones from fetal tissue in order to
improve movement and the 185

187. Research
response to medications.  While many of
the implanted cells survived in
the brain and produced dopamine, this therapy
was associated with only modest
functional improvements, mostly in patients under
the age of 60. 
186

188. Research
Unfortunately, some of the people who received
the transplants developed
disabling dyskinesias that could not be relieved by
reducing antiparkinsonian
medications.
187

189. Research
Another type of cell therapy involves stem
cells.  Stem cells derived from embryos can
develop into any kind of cell
in the body, while others, called progenitor
cells, are more restricted. 
188

190. Research
One study transplanted neural progenitor cells
derived from human embryonic
stem cells into a rat model of PD.  The cells
appeared to trigger
improvement on several behavioral tests, although
relatively few of the
189

191. Research
transplanted cells became dopamine-producing
neurons.  Other researchers
are developing methods to improve the number of
dopamine-producing cells that
can be grown from embryonic stem cells in culture.
190

192. Research
Researchers also are exploring whether stem
cells from adult brains might be useful in treating
PD.  They have shown
that the brain's white matter contains multipotent
progenitor cells that can
191

193. Research
multiply and form all the major cell types of the
brain, including
neurons. 
Gene therapy is yet another approach to 192

194. Research
treating PD.  A study of gene therapy in non-
human primate models of PD is
testing different genes and gene-delivery
techniques in an effort to refine
this kind of treatment.  An early-phase
clinical study is also testing
193

195. Research
whether using the adeno-associated virus type 2
(AAV2) to deliver the gene for
a nerve growth factor called neurturin is safe for
use in people with PD. 
Another study is testing the safety of gene therapy
using AAV to deliver a gene
194

196. Research
for human aromatic L-amino acid
decarboxylase, an enzyme that helps convert
levodopa to dopamine in the brain.  Other
investigators are testing
whether gene therapy to increase the amount of
glutamic acid decarboxylase,
195

197. Research
which helps produce an inhibitory
neurotransmitter called GABA, might reduce
the overactivity of neurons in the brain that results
from lack of dopamine.
196

198. Research
is to use a vaccine to modify the immune system in
a way that can protect
dopamine-producing neurons.  One vaccine
study in mice used a drug called
copolymer-1 that increases the number of immune
T cells that secrete
197

199. Research
anti-inflammatory cytokines and growth factors.
The researchers injected
copolymer-1-treated immune cells into a mouse
model for PD. The vaccine
modified the behavior of supporting (glial) cells in
the brain so that their
198

200. Research
responses were beneficial rather than harmful. It
also reduced the amount of
neurodegeneration in the mice, reduced
inflammation, and increased production
of nerve growth factors. Another study delivered a
vaccine containing
199

201. Research
alpha-synuclein in a mouse model of PD and
showed that the mice developed
antibodies that reduced the accumulation of
abnormal alpha-synuclein. 
While these studies are preliminary, investigators
hope that similar approaches
might one day be tested in humans. 200

202. Research
In recent years, Parkinson's research has
advanced to the point that halting the progression
of PD, restoring lost
function, and even preventing the disease are all
considered realistic
goals.  While the ultimate goal of preventing
PD may take years to achieve, 201

203. Research
researchers are making great progress in
understanding and treating PD.
One of the most exciting areas of PD
research is genetics.  Studying the genes 202

204. Research
can help researchers understand both inherited
and sporadic cases of the disease.
Identifying gene defects can also help researchers
understand how PD occurs,
develop animal models that accurately mimic the
neuronal death in human PD,
203

205. Research
identify new drug targets, and improve diagnosis.
As discussed in the “What Genes are Linked
to Parkinson's Disease?" section, several genes
have been definitively 204

206. Research
linked to PD in some people.  Researchers
also have identified a number of
other genes that may play a role and are working
to confirm these
findings.  In addition, several chromosomal
regions have been linked to PD
205

207. Research
in some families.  Researchers hope to
identify the genes located in these
chromosomal regions and to determine which of
them may play roles in PD.
206

208. Research
information and DNA samples from hundreds of
families with PD and are
conducting large-scale gene expression studies to
identify genes that are
abnormally active or inactive in PD.  They
also are comparing gene
207

209. Research
activity in PD with gene activity in similar diseases
such as progressive supranuclear
palsy. 
Some scientists have found evidence that 208

210. Research
specific variations in the DNA of mitochondria –
structures in cells that
provide the energy for cellular activity — can
increase the risk of getting PD,
while other variations are associated with a
lowered risk of the disorder. They
209

211. Research
also have found that PD patients have more
mitochondrial DNA (mtDNA) variations
than patients with other movement disorders or
Alzheimer's disease. Researchers
are working to define how these mtDNA variations
may lead to PD.
210

212. Research
In addition to identifying new genes for
PD, researchers are trying to learn how known PD
genes function and how the
gene mutations cause disease.  For
example, a 2005 study found that the
211

213. Research
normal alpha-synuclein protein may help other
proteins that are important for
nerve transmission to fold correctly.  Other
studies have suggested that
the normal parkin protein protects neurons from a
variety of threats, including
212

214. Research
alpha-synuclein toxicity and excitotoxicity.
Scientists continue to study environmental
toxins such as pesticides and herbicides that can
cause PD symptoms in 213

215. Research
animals.  They have found that exposing
rodents to the pesticide rotenone
and several other agricultural chemicals can cause
cellular and behavioral
changes that mimic those seen in PD.  Other
studies have suggested that
214

216. Research
prenatal exposure to certain toxins can increase
susceptibility to PD in
adulthood. An NIH-sponsored program
called the Collaborative Centers
for Parkinson's Disease Environmental Research
(CCPDER) focuses on how
215

217. Research
occupational exposure to toxins and use of caffeine
and other substances may
affect the risk of PD.
Another major area of PD research involves 216

218. Research
the cell's protein disposal system, called the
ubiquitin-proteasome system. If
this disposal system fails to work correctly, toxins
and other substances may
build up to harmful levels, leading to cell
death.  The
217

219. Research
ubiquitin-proteasome system requires interactions
between several proteins,
including parkin and UCH-L1. Therefore, disruption
of the ubiquitin-proteasome
system may partially explain how mutations in
these genes cause PD.
218

220. Research
Other studies focus on how Lewy bodies form
and what role they play in PD.  Some studies
suggest that Lewy bodies are
a byproduct of degenerative processes within
neurons, while others indicate
219

221. Research
that Lewy bodies are a protective mechanism by
which neurons lock away abnormal
molecules that might otherwise be harmful. 
Additional studies have found
that alpha-synuclein clumps alter gene expression
and bind to vesicles within
220

222. Research
the cell in ways that could be harmful. 
Another common topic of PD research is
excitotoxicity – overstimulation of nerve cells that
leads to cell damage or 221

223. Research
death. In excitotoxicity, the brain becomes
oversensitized to the
neurotransmitter glutamate, which increases
activity in the brain. The dopamine
deficiency in PD causes overactivity of neurons in
the subthalamic nucleus,
222

224. Research
which may lead to excitotoxic damage there and in
other parts of the brain.
Researchers also have found that dysfunction of
the cells' mitochondria can
make dopamine-producing neurons vulnerable to
glutamate. 
223

225. Research
Other researchers are focusing on how
inflammation may affect PD. Inflammation is
common to a variety of
neurodegenerative diseases, including
PD, Alzheimer's disease, HIV-1-associated
224

226. Research
dementia, and amyotrophic lateral sclerosis.
Several studies have shown that
inflammation-promoting molecules increase cell
death after treatment with the
toxin MPTP. Inhibiting the inflammation with drugs
or by genetic engineering
225

227. Research
prevented some of the neuronal degeneration in
these studies.  Other
research has shown that dopamine neurons in
brains from patients with PD have
higher levels of an inflammatory enzyme called
COX-2 than those of people
226

228. Research
without PD.  Inhibiting COX-2 doubled the
number of neurons that survived
in a mouse model for PD.
Since the discovery that MPTP causes 227

229. Research
parkinsonian symptoms in humans, scientists have
found that by injecting MPTP
and certain other toxins into laboratory
animals, they can reproduce the brain
lesions that cause these symptoms. This allows
them to study the mechanisms of
228

230. Research
the disease and helps in the development of new
treatments.  They also
have developed animal models with alterations of
the alpha-synuclein and parkin
genes.  Other researchers have used genetic
engineering to develop mice
229

231. Research
with disrupted mitochondrial function in dopamine
neurons.  These animals
have many of the characteristics associated with
PD.
230

232. Research
characteristics that can reveal whether the disease
is developing or
progressing – are another focus of research. 
Such biomarkers could help
doctors detect the disease before symptoms
appear and improve diagnosis of the
231

233. Research
disease.  They also would show if
medications and other types of therapy
have a positive or negative effect on the course of
the disease.  Some of
the most promising biomarkers for PD are brain
imaging techniques.  For
232

234. Research
example, some researchers are using positron
emission tomography (PET) brain
scans to try to identify metabolic changes in the
brains of people with PD and
to determine how these changes relate to disease
symptoms.  Other
233

235. Research
potential biomarkers for PD include alterations in
gene expression.
Researchers also are conducting many
studies of new or improved therapies for 234

236. Research
(DBS) is now FDA-approved and has been used in
thousands of people with PD,
researchers continue to try to improve the
technology and surgical techniques
in this therapy.  For example, some studies
are comparing DBS to the best
235

237. Research
medical therapy and trying to determine which
part of the brain is the best
location for stimulation.  Another clinical
trial is studying how DBS
affects depression and quality of life. 
236

238. Research
Other clinical studies are testing whether
transcranial electrical polarization (TEP) or
transcranial magnetic stimulation
(TMS) can reduce the symptoms of PD. In TEP,
electrodes placed on the scalp are
237

239. Research
used to generate an electrical current that
modifies signals in the brain's
cortex.  In TMS, an insulated coil of wire on
the scalp is used to
generate a brief electrical current.
238

240. Research
One of the enduring questions in PD
research has been how treatment with levodopa
and other dopaminergic drugs
affects progression of the disease. 
Researchers are continuing to try to
clarify these effects.  One study has
suggested that PD patients with a 239

241. Research
low-activity variant of the gene for COMT (which
breaks down dopamine) perform
worse than others on tests of cognition, and that
dopaminergic drugs may worsen
cognition in these people, perhaps because the
reduced COMT activity causes
240

242. Research
dopamine to build up to harmful levels in some
parts of the brain.  In the
future, it may become possible to test for such
individual gene differences in
order to improve treatment of PD.
241

243. Research
A variety of new drug treatments are in
clinical trials for PD.  These include a drug
called GM1 ganglioside that
increases dopamine levels in the brain. 
Researchers are testing whether
242

244. Research
this drug can reduce symptoms, delay disease
progression, or partially restore
damaged brain cells in PD patients.  Other
studies are testing whether a
drug called istradefylline can improve motor
function in PD, and whether a drug
243

245. Research
called ACP-103 that blocks receptors for the
neurotransmitter serotonin will
lessen the severity of parkinsonian symptoms and
levodopa-associated
complications in PD patients. Other topics of
research include
244

246. Research
controlled-release formulas of PD drugs and
implantable pumps that give a
continuous supply of levodopa.
Some researchers are testing potential 245

247. Research
neuroprotective drugs to see if they can slow the
progression of PD.  One
study, called NET-PD (Neuroexploratory Trials in
Parkinson's Disease), is
evaluating minocycline, creatine, coenzyme
Q10, and GPI-1485 to determine if
246

248. Research
any of these agents should be considered for
further testing.  The NET-PD
study may evaluate other possible neuroprotective
agents in the future. 
Drugs found to be successful in the pilot phases
may move to large phase III
247

249. Research
trials involving hundreds of patients.  A
separate group of researchers is
investigating the effects of either 1200 or 2400
milligrams of coenzyme Q10 in
600 patients.   Several MAO-B inhibitors,
including selegiline,
248

250. Research
lazabemide, and rasagiline, also are in clinical trials
to determine if they
have neuroprotective effects in people with PD.
Nerve growth factors, or neurotrophic 249

251. Research
factors, which support survival, growth, and
development of brain cells, are
another type of potential therapy for PD. 
One such drug, glial cell
line-derived neurotrophic factor (GDNF), has been
shown to protect dopamine
250

252. Research
neurons and to promote their survival in animal
models of PD.  This drug
has been tested in several clinical trials for people
with PD, and the drug
appeared to cause regrowth of dopamine nerve
fibers in one person who received
251

253. Research
the drug.  However, a phase II clinical study
of GDNF was halted in 2004
because the treatment did not show any clinical
benefit after 6 months, and
some data suggested that it might even be
harmful.  Other neurotrophins
252

254. Research
that may be useful for treating PD include
neurotrophin-4 (NT-4), brain-derived
neurotrophic factor (BDNF), and fibroblast growth
factor 2 (FGF-2).
253

255. Research
dietary supplements can slow PD, several clinical
studies are testing whether
supplementation with vitamin B12 and other
substances may be helpful. A 2005
study found that dietary restriction — reducing the
number of calories normally
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consumed – helped to increase abnormally low
levels of the neurotransmitter
glutamate in a mouse model for early PD. 
The study also suggested that
dietary restriction affected dopamine activity in
the brain.  Another
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study showed that dietary restriction before the
onset of PD in a mouse model
helped to protect dopamine-producing
neurons. 
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that might improve some of the secondary
symptoms of PD, such as depression and
swallowing disorders.  One clinical trial is
investigating whether a drug
called quetiapine can reduce psychosis or agitation
in PD patients with
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dementia and in dementia patients with
parkinsonian symptoms. Some studies also
are examining whether transcranial magnetic
stimulation or a food supplement
called s-adenosyl-methionine (SAM-e) can alleviate
depression in people with
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PD, and whether levetiracetam, a drug approved to
treat epilepsy, can reduce
dyskinesias in Parkinson's patients without
interfering with other PD drugs.
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implant cells to replace those lost in the
disease.  Researchers are
conducting clinical trials of a cell therapy in which
human retinal epithelial
cells attached to microscopic gelatin beads are
implanted into the brains of
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people with advanced PD.  The retinal
epithelial cells produce
levodopa.  The investigators hope that this
therapy will enhance brain
levels of dopamine.
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Starting in the 1990s, researchers
conducted a controlled clinical trial of fetal tissue
implants in
people with PD. They attempted to replace
lost dopamine-producing neurons
with healthy ones from fetal tissue in order to
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response to medications.  While many of
the implanted cells survived in
the brain and produced dopamine, this therapy
was associated with only modest
functional improvements, mostly in patients under
the age of 60. 
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Unfortunately, some of the people who received
the transplants developed
disabling dyskinesias that could not be relieved by
reducing antiparkinsonian
medications.
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Another type of cell therapy involves stem
cells.  Stem cells derived from embryos can
develop into any kind of cell
in the body, while others, called progenitor cells,
are more restricted. 
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One study transplanted neural progenitor cells
derived from human embryonic
stem cells into a rat model of PD.  The cells
appeared to trigger
improvement on several behavioral tests, although
relatively few of the
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transplanted cells became dopamine-producing
neurons.  Other researchers
are developing methods to improve the number of
dopamine-producing cells that
can be grown from embryonic stem cells in culture.
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Researchers also are exploring whether stem
cells from adult brains might be useful in treating
PD.  They have shown
that the brain's white matter contains multipotent
progenitor cells that can
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multiply and form all the major cell types of the
brain, including
neurons. 
Gene therapy is yet another approach to 269

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treating PD.  A study of gene therapy in non-
human primate models of PD is
testing different genes and gene-delivery
techniques in an effort to refine
this kind of treatment.  An early-phase
clinical study is also testing
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whether using the adeno-associated virus type 2
(AAV2) to deliver the gene for
a nerve growth factor called neurturin is safe for
use in people with PD. 
Another study is testing the safety of gene therapy
using AAV to deliver a gene
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for human aromatic L-amino acid
decarboxylase, an enzyme that helps convert
levodopa to dopamine in the brain.  Other
investigators are testing
whether gene therapy to increase the amount of
glutamic acid decarboxylase,
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which helps produce an inhibitory
neurotransmitter called GABA, might reduce
the overactivity of neurons in the brain that results
from lack of dopamine.
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is to use a vaccine to modify the immune system in
a way that can protect
dopamine-producing neurons.  One vaccine
study in mice used a drug called
copolymer-1 that increases the number of immune
T cells that secrete
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anti-inflammatory cytokines and growth factors.
The researchers injected
copolymer-1-treated immune cells into a mouse
model for PD. The vaccine
modified the behavior of supporting (glial) cells in
the brain so that their
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responses were beneficial rather than harmful. It
also reduced the amount of
neurodegeneration in the mice, reduced
inflammation, and increased production
of nerve growth factors. Another study delivered a
vaccine containing
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alpha-synuclein in a mouse model of PD and
showed that the mice developed
antibodies that reduced the accumulation of
abnormal alpha-synuclein. 
While these studies are preliminary, investigators
hope that similar approaches
might one day be tested in humans. 277