Parkinsons
treatment of parkinsons
L-dopa
SOD-1
definition and role in ALS
antioxidant that normally reduces oxidative stress
familial ALS: SOD1 mutation --> increase oxidative stress
T/F MS is characterized by autoreactive T and B cells crossing the blood-brain barrier
True
what are the 3 forms of alzheimers
nonhereditary sporadic
early onset familial
early onset
masked facies is a clinical manifestation of
parkinsons
Cellular changes include ___ of ____ in the ___. The decrease in ___ causes the patient to be unable to ___
apoptosis, dopamine-producing neurons, substantia nigra. dopamine secretion, control movement
definition of ALS
neurodegenerative disorder
involves lower and upper motor neurons
results in progressive muscle weakness
T/F MS is a chronic inflammatory progressive disease involving degeneration of PNS myelin, scarring, and loss of axons
False
CNS myelin
T/F ApoE4 is always truncated in Alzheimer patients and leads to cytoskeleton destabilization
Pathophysiology of Tau proteins and its function
stabilize microtubules
defective --> tangles --> interferes with axonal transport
cardinal manifestation
bradykinesia
muscle atrophy and further neurologic impairments caused by
apoptosis of neurons
neuroinflammation + excitotoxicity + oxidative stress + mitochondrial dysfunction
activated T cells attack ___ which exposes the ___ and disrupts ____ _____
myelin, axon, nerve conduction
Definition of Alzheimers
irreversible, progressive brain disorder
slowly destroys memory, thinking skills, and ability to carry out simple tasks
treatment of MS is mainly to
prevent exacerbations and permanent neurologic damage
unopposed cholinergic activity promotes ___ and dopamine deficiency, which causes ____, leads to uncontrollable resting tremors, rigidity, and/or bradykinesia
muscle tone, loss of normal inhibition of muscle tone
2 clinical manifestations
focal muscle weakness (arms and legs)
muscle atrophy
spasticity
loss of manual dexterity
difficulty swallowing/speaking
CSF biomarkers would show
IgG, immunoglobulins (antibodies)
Pathology of Amyloid precursor protein and its function
synapse formation
APP molecule --> proteolysis --> B amyloid --> (aggregate) plaques --> plaques on outside of nerve cell --> impair signal transduciton
initial stage of parkinsons shows
asymmetry
ex. decreased arm swing on one side
genetic predisposition/alteration
lewy body formation in neurons surrounding or w/in nervous system --> proteins misfolding and accumulation of a-synuclein
lewy body: accumulation of abnormal proteins in nerve cells
leads to dopamine neurodegeneration in basal ganglia
Cause of muscle spasticity
glutamate excitotoxicity
impaired glutamate intake at astrocyte
excess glutamate excites neuron when we don't want it
pathophysiology of T/B cells
T cell in blood --> cross BBB --> recognize myelin fragment that has been presented to T cell --> release of cytokines --> T cell re-entry into circulation --> calls in more Th and cytotoxic T cells
3 clinical manifestations
mild cognitive impairment
visuospatial deficits
memory loss
progressive --> forgetful, anxious, hostile
Urinary incontinence is a clinical manifestation of what neurologic disorder
multiple sclerosis