ILE 2 Exam 2, 217Study Questions with Correct Answers

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ILE 2 Exam 2, 217Study Questions with Correct Answers What are the three common forms of dementia? >>>Alzheimer's disease, vascular dementia, Lewy body dementia. What is the epidemiology of AD? (How many people, what percent of dementia cases) >>>5 million Americans, 60-80% of all dementia cases Who is affected by early onset AD, what age? >>>< 65 y/o, early as 30 with down syndrome Who is affected by late onset AD, what age? >>>> 65 y/o, age may suggest etiology What is the life expectancy of AD after diagnosis? >>>4 to 8 years What are the three chromosomes related to early onset AD? >>>C14, C1, C21 How is C14 related to early onset AD? >>>Increased production of A-beta peptides, majority and most aggressive How is C1 related to early onset AD? >>>Increase production of A-beta peptides How is C21 related to early onset AD? >>>Extra copy causes down syndrome, leading to an increase in APP cause an increase in A-beta peptides What genotype, in general, is related to late onset AD? >>>APOE What effect does APOE2 have on late onset AD? >>>Protective, E2/E2 less likely to develop AD What effect does APOE3 have on late onset AD? >>>Having E3/E3 is average risk for AD What effect does APOE4 have on late onset AD? >>>Little to no protective effects. E4/E4 most likely to develop AD. Causes systemic and brain effects. Increase A-beta aggregation and decreased clearance. Decreased lipid/cholesterol metabolism, decreased inflammatory response. What are risk factors for developing AD? >>>Age, FH, head injury, number of depressive episodes, MCI, decreased brain capacity, anything decreasing blood to brain, TBI, mid-life obesity, HTN, smoking, diabetes, hyperlipidemia What are the 3 hallmark signs of AD? >>>Extracellular amyloid plaques, intracellular neurofibrillary tangles, neuronal loss What are intracellular neurofibrillary tangles composed of? >>>Hyperphosphorylated tau deposited in the neuron. What is the amyloid cascade hypothesis? >>>Imbalance between production and clearance of A-beta peptide causes aggregation and accumulation of A-beta, usually in early onset and autosomal cases. What is the amyloidogenic pathway? >>>Normally have APP-AB-APP. AB is cleaved by beta-secretase from APP until free A-beta due to mutation. A-beta accumulates into amyloid plaques causeing altered APP processing. Leads to excess beta-amyloid neurotoxicity, tau phosphorylation Formation of plaques synapse loss and change in NT leading to loss of function (dementia) What three things can lead to A-beta aggregation and accumulation? >>>Altered A-beta, normal A-beta and APOE4, normal A-beta and aging. What is the outcome of A-beta aggregation and accumulation? What does it cause? >>>Toxicity, neuronal death, and loss of function. What is the effect of neuroinflammation on AD? >>>Risk factors for AD increase immune activation by local or systemic inflammation causing enhancement of microglial activation. Process: pro-inflammatory mediators and decrease A-beta clearance activation microglial cells systemic inflammation increased microglial cell activation What is the cholinergic hypothesis for AD? >>>Ach is important for memory. Loss of Ach increase AD severity. Impaired choline uptake, decrease Ach release, deficits in nicotinic and muscarinic receptors.

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