BMS 310 EXAM
#2 SCORED A+
BMS 310
Evatee 9/8/24 BMS 310
,BMS 310 EXAM #2 SCORED A+
clinical manifestations of AD Answer - dementia, alterations in behavior and
personality
dementia Answer - deterioration of memory and cognition
brain of AD Answer - narrowed gyri and widened sulci due to nueronal loss
frontal lobe impairment in AD Answer - cognition, personality, and social
behavior changes
temporal lobe impairment in AD Answer - changes in memory due to nueron
loss in the hippocampus
biochemical pathology of AD Answer - depletion of ACh, very noticable loss
cholnergic nuerons
basal nucleus of Meynert area Answer - where most ACh is provided and
spreads it through out the brain
AChase inhibitors Answer - used to increase the ACh levels in CNS and shown
to improve measurements of thinking, ADLs, and behavior
Examples of Achase inhibitors Answer - Cognex (tacrine)
Aricept (donepezil)
, Exelon (rivastigamine)
Reminyl (galantamine
Glutamate NMDA receptor anatagonist Answer - memantine (Namenda)
blocks glutamate receptors
experimental approaches to AD Answer - beta amyloid vaccine
gamma secretase inhibitors
2 hallmark lesions of AD Answer - Nuerofibrillary tangles
Nueritic plaque
Neurofibrillary tangles Answer - intranueral accumulations of insoluble, paired
helical filament
derived from cytoskeleton protein, tau
start to reinforce dying or injury nuerons
over-accumlate and clog cytoplasmic compartment
Nueritic plaques Answer - insoluble, extracellular acculations in cerebral cortex
beta-amyolid protein Answer - composed of 42 amino acids
derived from abnormal 700 amino acid peptide
beta-amyloid precursor Answer - 700 abnormal amino acid peptide
enzymes beta-secretase and gamma secretase
cell surface receptor/ cell adhesion molecule
#2 SCORED A+
BMS 310
Evatee 9/8/24 BMS 310
,BMS 310 EXAM #2 SCORED A+
clinical manifestations of AD Answer - dementia, alterations in behavior and
personality
dementia Answer - deterioration of memory and cognition
brain of AD Answer - narrowed gyri and widened sulci due to nueronal loss
frontal lobe impairment in AD Answer - cognition, personality, and social
behavior changes
temporal lobe impairment in AD Answer - changes in memory due to nueron
loss in the hippocampus
biochemical pathology of AD Answer - depletion of ACh, very noticable loss
cholnergic nuerons
basal nucleus of Meynert area Answer - where most ACh is provided and
spreads it through out the brain
AChase inhibitors Answer - used to increase the ACh levels in CNS and shown
to improve measurements of thinking, ADLs, and behavior
Examples of Achase inhibitors Answer - Cognex (tacrine)
Aricept (donepezil)
, Exelon (rivastigamine)
Reminyl (galantamine
Glutamate NMDA receptor anatagonist Answer - memantine (Namenda)
blocks glutamate receptors
experimental approaches to AD Answer - beta amyloid vaccine
gamma secretase inhibitors
2 hallmark lesions of AD Answer - Nuerofibrillary tangles
Nueritic plaque
Neurofibrillary tangles Answer - intranueral accumulations of insoluble, paired
helical filament
derived from cytoskeleton protein, tau
start to reinforce dying or injury nuerons
over-accumlate and clog cytoplasmic compartment
Nueritic plaques Answer - insoluble, extracellular acculations in cerebral cortex
beta-amyolid protein Answer - composed of 42 amino acids
derived from abnormal 700 amino acid peptide
beta-amyloid precursor Answer - 700 abnormal amino acid peptide
enzymes beta-secretase and gamma secretase
cell surface receptor/ cell adhesion molecule
