PHA 3112 Study Guide - Midterm Guide: Mild Cognitive Impairment, Nmda Receptor, Partial Seizure

• School: University of Ottawa
• Department: Pharmacology
• Course: PHA 3112
• Professor: Pierre Fortier

Document Summary

Al)chemi)er"s disease (cid:894)ad(cid:895): (cid:272)hara(cid:272)terized (cid:271)y progressi(cid:448)e (cid:373)e(cid:373)ory loss, i(cid:373)paired thi(cid:374)ki(cid:374)g, neuropsychiatric symptoms (hallucinations, delusions) & inability to perform routine tasks of daily living, Fatal disease; no cure; no way to regenerate loss neurons in the brain: pathophysiology of alzhiemer"s disease: etiology (cause): unknown. Degeneration of neurons: begins at hippocampus (role in memory) . Cerebral cortex (central to speech, perceptions, reasoning, & other higher functions). Eventually causes the brain function to cause death because of the complete. Degeneration of cortical neurons: reduced cholinergic transmission: ad(cid:448)a(cid:374)(cid:272)ed ad = a(cid:272)h. Important transmitter in hippocampus & cerebral cortex neuronal degeneration occurs: ach important for formation of memories linked to memory loss. Beta-amyloid: protein fragment, surrounded by the remnants of dead axons& dendrites, hallmark of ad. Neuritic plaques: found in hippocampus & cerebral cortex, hallmark of ad. Neurofibrillary tangles: form inside neurons result when microtubulas formation ebcoems disrupted from ad. Cause of this is tau protein that forms cross- bridges between microtubules in healthy neurons.