AD set 4

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  1. what accounts for 85% of brain's weight?
    cerebral hemispheres
  2. corpus callosum
    connects two cerebral hemispheres
  3. what is the cerebral hemisphere covered by?
    outer layer called cerebral cortex
  4. what is function of cerebellum
    • balance and coordination
    • 10% of brain 
    • 2 hemispheres
    • receives info from eyes, ears and muscles about movements and position
  5. brain stem
    • connects the spinal cord with brain
    • relay messages to and from organs
    • controls automatic function (heart rate, blood pressure, breathing)
  6. hippocampus
    short term memories to long term
  7. thalamus
    receives sensory and limbic info and sends to cerebral cortex
  8. hypothalamus
    neurotransmitters to monitor and control body functions (internal clock)
  9. limbic system
    controls emotions and instinctive behavior
  10. what does PET stand for, what does it do?
    • positron emission tomography 
    • pairs of gamma rays emitted by tracer (fludeoxyglucose, glucose analogue) detected as a function of position and time, thus signaling metabolic activity
  11. what does T1w/T2w ration reveal?
    myelin content (lipids vs free and bound water)
  12. pathological and physical signs of advanced AD
    • extreme shrinkage in hippocampus and cerebral cortex
    • enlarged ventricles
  13. what are preserved abilities in memory?
    • long ago memories
    • confabulation
    • emotional memories
    • motor memories
  14. what are preserved abilities of understanding
    • can get facial expression
    • hears tone of voice
    • gets some non-verbal cues
  15. preserved languages
    • singing
    • automatic speech
    • swearing
  16. perserved emotional abilities
    desires to be respected, in control and regrets after action
  17. where to b-amyloid plaques accumulate
    outside and around nerve cells
  18. where do neurofibrillary tangles form?
    twisted fibers that build up inside nerve cell
  19. what form PHF?
    phosphorylated tau
  20. why is tau important
    stabilizes microtuble, part of cell's transport system
  21. what kind of protein is APP
    one pass TM protein in neurons
  22. how does tau become dysfunctional in AD
    becomes hyperphosphorylated (MT collapse) and assemble into spirals (PHF) which forms NFT that lead to cell death
  23. what are the proposed ab and tau modes of interaction?
    • AB leads to hyperphosphorylation of tau
    • tau mediates AB toxicity
    • ab and tau act together, amplifying individual toxcities
  24. what is the tau axis hypothesis
    • initiation of ab formation in brain (MCI)
    • low levels of denderitic tau are associated with limited vulnerability of neurons to synaptic amyloid beta toxicity
    • ab induced toxicity causes high phos tau in neurons as disease progresses (tau increase in dendrite)
    • progressively increasing levels of dendritic tau make neurons vulnerable to b-amyloid toxicity in postsynaptic compartment
    • which further increase tau phos and somatodendritic accumulation (cycle)
  25. what is the weight of soluble ab
  26. what are risk factors for AD
    • free radicals (oxidative damage)-> neuronal injury
    • homocysteine increased in AD (also in heart diseases)
    • inflammation and strokes
  27. what are two processes occurring in in AD
    • cells are shrinking and dying
    • cells are producing less chemicals to send messages
  28. what is the synaptic cleft look like for AD patients
    • loss of neurons results in less NT
    • greater distance between cells
    • AChE hydrolyze them before sufficient number of ACh molecules can deliver their message
  29. what are the two major hypothesis for AD
    • baptists
    • tauists
  30. BAPtists
    amyloid b42 accumulation leads to formation of plaques
  31. Tauists
    phis makes them sticky, break up of MT, loss of axonal transport causes death
  32. amyloid hypothesis
    • APP broken down
    • nonsoluble fragment (AB42 accumulates) and deposited outside the cell
    • plaques
  33. what are PSEN1 genes for
    presenilins (subunits of y-secretase)
  34. what is APP originally for?
    neuronal growth, survival and repair
  35. where does y and b-secretases cut?
    • B-secretase (outside)
    • y-(in membrane)
  36. how does b-amyloid aggregate?
    self aggregate and attracts other materials to form plaque
  37. which mutation on APP has protective effect when you have one copy of it
  38. what is the dutch mutation
    blood level increase in AB, weakening of cerebral blood vessels, more diffuse plaques
  39. type 1 AD
    • several mutations in APP gene on chromosome 1
    • most common Val717Iso
    • abnormal ab fragment
    • 15-20% fAD
    • autosomal dominant
  40. type 3 AD
    • mutations in PSEN1 on chromosome 14
    • lead to aa substitution
    • overproduction of ab fragment
    • 30-70 fAD
  41. type 4 AD
    • mutations in PSEN2 on chromosome 1
    • 2 alleles (Asn141Iso and Met239Val)
    • overproduction of ab fragment
    • less 5% fAD
  42. type 2 AD
    • epsilon 4 allele of ApoE gene on chromosome 19 confers risk
    • epsilon 2 of ApoE gene on chromosome 19 confers protection
    • unclear mechanism
    • ApoE is very low density lipoprotein that transports cholesterol
    • most cases are late
  43. primary prevention
    • delay onset of AD pathology
    • decrease ab 42 production
    • prevent tangle formation
  44. secondary prevention
    • delay onset of MCI individuals with pathology
    • decrease accumulated ab burden
    • decrease neurodegeneration with anti-tau or neuroprotective agents
  45. tertiary prevention and treamtent
    • delay onset or progression of dementia
    • neuroprotection-prevent neuronal loss
    • enhance function of remaining neurons
    • neurotransmitter repletion
Card Set:
AD set 4
2015-10-01 20:14:27

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