Neurological AD

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  1. 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)
  2. choline acetyltransferase
    responsible for the synthesis of acetylcholine
  3. CNS abnormalities are assessed by?
    levels of AB decrease and tau increase in CSF
  4. what chromosome is APP encoded on?
  5. mutations on APP and PS2 affect what?
    BACE (beta site APP cleaving enzyme 1)
  6. role of y secretes
    generate N and C termini of AB peptides
  7. APPswe
    double mutation to enhance BACE cleavage at N terminus of AB resulting in elevation of all AB peptides
  8. what is the catalytic site of y-secretase
  9. mutations of y-secretase
    increase AB 42 peptides
  10. PHF
    paired helical fragment, aggregated b-pleated sheet assemblies of tau protein
  11. plaques are surrounded by?
    astrocytes and microglial
  12. PET and SPECT shows what?
    decreased glucose utilization, reduced in regional blood flow in parietal and temporal lobes
  13. parietal lobe
    spatial sense and navigation
  14. temporal lobe
    processing sensory input into language
  15. pittsburg compound B
    binds to AB and used to visualize AB amyloid burden in vivo
  16. fMRI
    show brain atrophy (hippocampus and entorhinal cortex)
  17. entorhinal cortex
    memory consolidation
  18. F-FDDNP
    binds to NFT, higher retention in hippocampus and in amygdala
  19. spectroscopy
    shows decrease in N-acetyl-asparatate (marker of neural density and viability) and increased myoinosital (gliosis)
  20. gliosis
    proliferation of glial cells (inflammation)
  21. EEG
    reduced amplitude in alpha and beta (reduced excitability of cortical neurons showing loss of cholinergic innervation
  22. mermantine
    • sustained over activation of NMDA glutamate receptors, while impairs plasticity and leads to neuronal degeneration
    • mermantine reduces level of activation
  23. SSRI
    selective serotonin reuptake inhibitors
  24. anxioloytic
    anxiety inhibitor
  25. NSAIDS
    activation of COX and modulation of y-secretase
  26. statin
    cholesterol lowering drugs
  27. GSK-3 inhibitor
    lithium, inhibits tau protein hyperphosphorylation
  28. BACE
    transmembrane aspartyl proteases
  29. lewy body
    altered forms of tangle found in people that lack AB plaques
  30. MCI
    transitional stage between normal aging and early AD
  31. ApoE
    • carries cholesterol and other lipids in the blood
    • 60% of patients with AD have one APOE4 allele
  32. limbic system
    emotion, behavior, motivation
  33. circuits damaged by AD
    • basal forebrain cholinergic system
    • monoamine neurons in brain steam
    • hippocampus
    • entorhinal cortex
    • limbic cortex 
    • neocortex (sight and hearing)
  34. where do AB peptides tend to accumulate?
    in the extracellular space of the neuropile of the neocortex and hippocampus
  35. where do AB42 multimers accumulate?
    at nerve terminals
  36. first case of AD reported
  37. what enzyme is active in the catabolism of ABeta
    • IDE (insulin degrading enzyme)
    • variants of IDE may predispose to the disease
  38. why are abeta plaques neurotoxic?
    microglial activation and neuritic degeneration
  39. what is the main gross anatomical correlate of AD
    progressive cortical atrophy
  40. basal nucleus of Meynert
    where cholinergic neurons are located
  41. disintegration of semantic memory
    • mild AD
    • damage and reduce cholinergic innervation to the temporal neocortex
    • test of word list generation by semantic category
  42. 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
  43. perceptual priming
    implicit memory from prior exposure to perceptual features of an object.
  44. 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
  45. ideational apraxia
    impaired knowledge of actions
  46. ideomotor apraxia
    • deficits in transcoding the concept of a motor sequence into corresponding actions
    • 1/3 of early AD patients
  47. constructive apraxia
    • inability to combine given elements into a meaningful whole
    • presence in early stage predicts rapid cognitive decline
  48. depression
    • altered density of serotonin receptors in frontal and temporal cortical regions. 
    • reduced perfusion and glucose metabolism in frontal lobe
  49. amyloid depression
    altered beta 42/beta 40 ratio
  50. cognitive anosognosia
    unawareness of cognitive symptoms
  51. diagnosis of AD
    presence of clinically significant cognitive impairment with gradual con set and without secondary causes of dementia
  52. what is helpful in differentiating semantic dementia and AD
    paired associate learning test highlight acquisition impairments specific to AD
  53. clock test
    reveal spatial memory, attentional and apraxic defects
  54. working memory can be assessed using?
    letter number sequencing, forward and backward digit span
  55. intrusion error
    memory that never occurred, or remembering it in different way
  56. n-acetylaspartate
    marker of neural density and viability
  57. H-MRS (Spect)
    • shows decrease in N-acetylasparatate
    • increase in myoinosital (marker of gliosis)
  58. tarenflurbil
    most advanced y-secretase modulator
  59. tramiprosate
    interfere with abet and glycosaminoglycans that promote abeta aggregation
  60. senile dementia
    progressive cognitive decline after middle age
  61. features of neuritic plaques, diffuse (preamyloid plaques)
    lack surrounding dystrophic neurites and altered microglial and astrocytes
  62. AD brain regions not strongly implicated in clinical syndrome
    thalamus and cerebellum
  63. 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
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Neurological AD
2015-09-15 13:51:14

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