synuclein:protein inneuronal and glial cell that can
aggregate and form Lewy bodies; these aggregates
generate death of neurons;
mutations of the a-synuclein gene in 4q21 or the
occurrence of duplication or triplicate of the normal
synuclein gene;
mutations of leucine-rich 2 com rescan(LRRK2) and the
UCHL1 gene can also cause autosomal dominant
parkinsonism;
happens loss of pigmented neurons of the black
substance, locusand cereum and other groups of
cisdopamine squid is rgics of the brainstem if
ofgeneram;the loss ofneurons of the black substance
results in the depletion of dopamine;
NEURODEGENERATIVE
onset between 21 and 40 years of age is called young PD
DISEASES - or early start -> the geneticcausesare morelikely in
juvenile PD and early start -> these fo rmas may be
PARKINSON's different from late-onsetPD because they progress more
slowly andare only sensitive to dopamine
tremor -> rhythmic oscillatory movement around a -> at treatmentsand becausemost of the deficiency results
rest is characteristic of parkinsonism; from non-motor symptoms such as depression, anxiety
-non-> involuntary, unpredictable and irregular muscle and pain;
contractions that occur in different parts of the body and
impair voluntary activity; smoking, coffee consumption, the use of anti-
slow and contortion -> atetose; inflammatory drugs and the presence of high serum levels
prolonged to the point of being more adequately regarded of uric acid are protective;
as abnormal postures -> dystonia increased incidence of the disease in individuals working
-tics -> abnormal movements coordinated and in the academic, health care or agriculture area, as well
suddenthose that tend to occurrepetitively, especially on as in those withexposure to lead or manganese or with
the face and head, vitamin D deficiency;
is a combination of rigidez, bradykinesia (slow and secondary parkism:
decreased movements), tremor and postural or gait • brain dysfunction characterized by dopaminergic block
instability; of the basal ganglia and that is similar to PD, but the
cause is something more than PD (e.g.,fmacos,
cognitive decline occurs in many patients with disease cerebrovascular disease, trauma, post-encephalitic
proaggression + affective disorders (anxiety or changes);
depression), personality changes, abnormalities of • the mechanism is blockade or interference in the action
autonomous function (sphincter or sexual functions; of dopamine in the basal gânglios ;
suffocation; sweating abnormalities; disorders of blood • the most common cause is the use of drugs that
pressure regulation), sleep disorders decrease dopamine activityisrgica;
andsensorycomplaints or pain;
TREATMENT
in general, the disease is progressive, resulting in
• CARBIDOPA/LEVODOPA: more effective
increasing disability, unless effective treatment is insated;
treatment; levodopa is the metab olic precursor
of dopamine,crosses the blood brain barrier,goes
PATHOGENESIS
to the basal ganglia, where it is decarboxylada to
combination of reduced protein degradation, form dopamine;
accumulation and aggregation - co-administration with perifinhibitorisrich in
of intracellular proteins, descarboxilase, carbidopa, prevents
oxidative stress, mitochondrial levodopa from being decarboxylada in
injury, inflammatory cascades dopamine outside the cisrebro (in
and apoptosis; theperiphery), thus reducing the necessary
doses of levodopa to produce therapeutic
genetic factors are important, levels in the cis rebro and minimizing adverse
especially when the disease effects;
occurs in patients under 50
years of age; • amantadine,type B MAO inhibitor (MAO-B) or, in
some patients, anticholinergic drugs; may
aggregate and form Lewy bodies; these aggregates
generate death of neurons;
mutations of the a-synuclein gene in 4q21 or the
occurrence of duplication or triplicate of the normal
synuclein gene;
mutations of leucine-rich 2 com rescan(LRRK2) and the
UCHL1 gene can also cause autosomal dominant
parkinsonism;
happens loss of pigmented neurons of the black
substance, locusand cereum and other groups of
cisdopamine squid is rgics of the brainstem if
ofgeneram;the loss ofneurons of the black substance
results in the depletion of dopamine;
NEURODEGENERATIVE
onset between 21 and 40 years of age is called young PD
DISEASES - or early start -> the geneticcausesare morelikely in
juvenile PD and early start -> these fo rmas may be
PARKINSON's different from late-onsetPD because they progress more
slowly andare only sensitive to dopamine
tremor -> rhythmic oscillatory movement around a -> at treatmentsand becausemost of the deficiency results
rest is characteristic of parkinsonism; from non-motor symptoms such as depression, anxiety
-non-> involuntary, unpredictable and irregular muscle and pain;
contractions that occur in different parts of the body and
impair voluntary activity; smoking, coffee consumption, the use of anti-
slow and contortion -> atetose; inflammatory drugs and the presence of high serum levels
prolonged to the point of being more adequately regarded of uric acid are protective;
as abnormal postures -> dystonia increased incidence of the disease in individuals working
-tics -> abnormal movements coordinated and in the academic, health care or agriculture area, as well
suddenthose that tend to occurrepetitively, especially on as in those withexposure to lead or manganese or with
the face and head, vitamin D deficiency;
is a combination of rigidez, bradykinesia (slow and secondary parkism:
decreased movements), tremor and postural or gait • brain dysfunction characterized by dopaminergic block
instability; of the basal ganglia and that is similar to PD, but the
cause is something more than PD (e.g.,fmacos,
cognitive decline occurs in many patients with disease cerebrovascular disease, trauma, post-encephalitic
proaggression + affective disorders (anxiety or changes);
depression), personality changes, abnormalities of • the mechanism is blockade or interference in the action
autonomous function (sphincter or sexual functions; of dopamine in the basal gânglios ;
suffocation; sweating abnormalities; disorders of blood • the most common cause is the use of drugs that
pressure regulation), sleep disorders decrease dopamine activityisrgica;
andsensorycomplaints or pain;
TREATMENT
in general, the disease is progressive, resulting in
• CARBIDOPA/LEVODOPA: more effective
increasing disability, unless effective treatment is insated;
treatment; levodopa is the metab olic precursor
of dopamine,crosses the blood brain barrier,goes
PATHOGENESIS
to the basal ganglia, where it is decarboxylada to
combination of reduced protein degradation, form dopamine;
accumulation and aggregation - co-administration with perifinhibitorisrich in
of intracellular proteins, descarboxilase, carbidopa, prevents
oxidative stress, mitochondrial levodopa from being decarboxylada in
injury, inflammatory cascades dopamine outside the cisrebro (in
and apoptosis; theperiphery), thus reducing the necessary
doses of levodopa to produce therapeutic
genetic factors are important, levels in the cis rebro and minimizing adverse
especially when the disease effects;
occurs in patients under 50
years of age; • amantadine,type B MAO inhibitor (MAO-B) or, in
some patients, anticholinergic drugs; may
