Biochem- Neuropsychiatric Disorders Flashcards
Which receptor does the antibodies target in myasthenia gravis?
NmAchR
Which subunit of the NmAchR does the antibodies target in Myasthenia Gravis?
α1-subunit
In Huntingtons, there is an excess release of which NT?
Glutamate
The excess glutamate in Huntingtons causes the binding of which receptor?
NMDA
The excess binding of the NMDA receptor causes a toxic influx of which ion?
Ca++
The excess Ca++ causes what in the nerve cell?
intracellular Ca++ activates nucleases, proteases and phospholipases –> cell death
How can strokes lead to cellular death by Ca++?
Ischemia from blockage or hemorrhage triggers glutamate release from oxygen-starved neurons –> toxic levels of Ca++ enter through the NMDA receptor –> this causes exocytosis of additional glutamate from the NMDA stimulated neuron (amplification) –> intracellular Ca++ activates nucleases, proteases and phospholipases –> cell death
The excess Ca++ in strokes causes the release of which 2 factors which worsens the disease?
platelet-activating factor and the release of arachidonic acid, which causes vasoconstriction, and thus worsens the thrombosis.
There is a degeneratiuon of which part of the brain in Parkinsons?
substantia nigra
Death of the substantia nigra causes a decreasse in which NT?
Dopamine
A decrease in DA causes an increase in what other NT?
Ach
To treat parkinsons, which drug(s) do you need?
A. Dopamine B. L-Dopa C. L-Dopa + carbidopa D. Physostigmine + L-Dopa E. Red red winnneeeeee. stay close to meeeeeee.
C. L-Dopa and carbidopa
Why do you need Carbidopa in addition to the L-dopa?
Otherwise L-dopa would be rapidly degraded by dopa decarboxylase in the periphery before it passes the BBB
Does carbidopa pass the BBB with L-dopa?
No.
What forms in the cortex and hippocampus in Alzheimers pts?
Amyloid plaques
What are amyloid plaques made of?
a clump of amyloid beta peptides (AbP)
Where are AbP’s derived from?
the proteolysis of amyloid precursor protein (APP)
What happens in neurofibillary tangles?
the helical filament stabilizer tau is modified, which tangles and kills the cell
How can AbP plaques cause excessive Ca++ stimulation?
AbP plaques are insoluble in the extracellular space where it is made from APP. It can therefore stimulate excessive Ca++, leading to the activation of protein kinases, induced phosphorylation of tau, and eventually cell death. AbP is therefore neurotoxic (kinda like glutamate for Huntingtons)!
Really good video: https://www.youtube.com/watch?v=NjgBnx1jVIU
Genereally, what happens with dopamine in schizophrenia?
there is evidence for excess dopamine production in schizophrenia by an icnrease in D2 activity
