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physiological responses of AD
- enlargement of ventricles
- atrophy of hippocampus
- degeneration of cholinergic neurons
- impairment of limb movement
- high incidence of depression (serotonin receptors decrease)
responsible for the synthesis of acetylcholine
CNS abnormalities are assessed by?
levels of AB decrease and tau increase in CSF
what chromosome is APP encoded on?
mutations on APP and PS2 affect what?
BACE (beta site APP cleaving enzyme 1)
role of y secretes
generate N and C termini of AB peptides
double mutation to enhance BACE cleavage at N terminus of AB resulting in elevation of all AB peptides
what is the catalytic site of y-secretase
mutations of y-secretase
increase AB 42 peptides
paired helical fragment, aggregated b-pleated sheet assemblies of tau protein
plaques are surrounded by?
astrocytes and microglial
PET and SPECT shows what?
decreased glucose utilization, reduced in regional blood flow in parietal and temporal lobes
spatial sense and navigation
processing sensory input into language
pittsburg compound B
binds to AB and used to visualize AB amyloid burden in vivo
show brain atrophy (hippocampus and entorhinal cortex)
binds to NFT, higher retention in hippocampus and in amygdala
shows decrease in N-acetyl-asparatate (marker of neural density and viability) and increased myoinosital (gliosis)
proliferation of glial cells (inflammation)
reduced amplitude in alpha and beta (reduced excitability of cortical neurons showing loss of cholinergic innervation
- sustained over activation of NMDA glutamate receptors, while impairs plasticity and leads to neuronal degeneration
- mermantine reduces level of activation
selective serotonin reuptake inhibitors
activation of COX and modulation of y-secretase
cholesterol lowering drugs
lithium, inhibits tau protein hyperphosphorylation
transmembrane aspartyl proteases
altered forms of tangle found in people that lack AB plaques
transitional stage between normal aging and early AD
- carries cholesterol and other lipids in the blood
- 60% of patients with AD have one APOE4 allele
emotion, behavior, motivation
circuits damaged by AD
- basal forebrain cholinergic system
- monoamine neurons in brain steam
- entorhinal cortex
- limbic cortex
- neocortex (sight and hearing)
where do AB peptides tend to accumulate?
in the extracellular space of the neuropile of the neocortex and hippocampus
where do AB42 multimers accumulate?
at nerve terminals
first case of AD reported
what enzyme is active in the catabolism of ABeta
- IDE (insulin degrading enzyme)
- variants of IDE may predispose to the disease
why are abeta plaques neurotoxic?
microglial activation and neuritic degeneration
what is the main gross anatomical correlate of AD
progressive cortical atrophy
basal nucleus of Meynert
where cholinergic neurons are located
disintegration of semantic memory
- mild AD
- damage and reduce cholinergic innervation to the temporal neocortex
- test of word list generation by semantic category
perform a fine motor skill and retina it for
- implicit memory is spared (previous experiences aid the performance of a task without conscious awareness of these previous experiences)
- sparing of neostriatal and cerebellar networks
implicit memory from prior exposure to perceptual features of an object.
what reflects dysfunctional supervisory control and response inhibition?
- difficulties in shifting attention from a task or object to another.
- demonstrated in tests with identifying overlapping line drawings and tests requiring selective focus or local or global visual features
impaired knowledge of actions
- deficits in transcoding the concept of a motor sequence into corresponding actions
- 1/3 of early AD patients
- inability to combine given elements into a meaningful whole
- presence in early stage predicts rapid cognitive decline
- altered density of serotonin receptors in frontal and temporal cortical regions.
- reduced perfusion and glucose metabolism in frontal lobe
altered beta 42/beta 40 ratio
unawareness of cognitive symptoms
diagnosis of AD
presence of clinically significant cognitive impairment with gradual con set and without secondary causes of dementia
what is helpful in differentiating semantic dementia and AD
paired associate learning test highlight acquisition impairments specific to AD
reveal spatial memory, attentional and apraxic defects
working memory can be assessed using?
letter number sequencing, forward and backward digit span
memory that never occurred, or remembering it in different way
marker of neural density and viability
- shows decrease in N-acetylasparatate
- increase in myoinosital (marker of gliosis)
most advanced y-secretase modulator
interfere with abet and glycosaminoglycans that promote abeta aggregation
progressive cognitive decline after middle age
features of neuritic plaques, diffuse (preamyloid plaques)
lack surrounding dystrophic neurites and altered microglial and astrocytes
AD brain regions not strongly implicated in clinical syndrome
thalamus and cerebellum
where are NFT found?
- intraneuronal cytoplasmic bundles of paired, helical wound
- in entorhinal cortex, hippocampal formation, amygdala, association cortices of frontal, temporal and parietal lobes