PBD 4 Alzheimers

Card Set Information

Author:
swynocker
ID:
50768
Filename:
PBD 4 Alzheimers
Updated:
2010-11-20 17:09:43
Tags:
PBD Alzheimers
Folders:

Description:
PBD 4 Alzheimers
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user swynocker on FreezingBlue Flashcards. What would you like to do?


  1. Who was the first alzheimers patient?
    August D, 51 years old
  2. T/F alzheimers is considered a common form of dementia.
    False, Rare (1890s-1980s)
  3. What is the most commmon neuro degenerative disease?
    Alzheimers
  4. Who is more likely to get alzheimers (gender wise)
    Women
  5. Florida has _#_ of dementia patients as of 2010
    450,000
  6. Sporadic AD represents what percent of cases. When is its onset age normally?
    • 90%
    • 65 y/o
  7. T/F familial AD is the most common case.
    False, 10%, age of onset is before 65 and is caused by APP, PS1, and PS2 genes.
  8. Three clinical stages of AD
    • Mild, moderate, and severe.
    • Daily activities not interfered
    • Daily activities significantly affected
    • Require total care
  9. Early stage AD shows a degeneration of _____ neurons. This results in what?
    • Hippocampal
    • short term memory loss
  10. Mid stage AD shows degeneration of ____ lobe and affects what?
    • Frontal lobe
    • affects judgement, safety awareness, planning and other complex thinking
  11. late stage AD neurogeneration spreads ______.
    EVERYWHERE
  12. Clinical tests to diagnose AD are
    • Mini mental state exam
    • CT, MRI, PET
    • and tests that can affect memory/cognition
  13. New clinical diagnosis for AD
    Imaging for amyloid plagques and tangles in brain
  14. T/F definitive diagnosis for AD can be done while someone is conscious.
    False, POST MORTEM!

    Cortical atrophy, ventricular dilation, amyloid plaques, tangles
  15. AD brains have _____ gyrus and a ____ sulcus. They also have a dilated _____.
    • Narrowed, widened
    • Ventricle
  16. Amyloid plaques are ___-cellular whereas neurofibrillary tangles are ____-cellular
    Extra, intra
  17. The core of amyloid plaques is made up of
    beta Amyloid peptides
  18. other components of amyloid plaques include
    • B-amyloid proteins
    • Apolipoprotein E
    • protease inhibitors
    • complement proteins
    • Metal irons
  19. APP stands for __ ___ ___. What are its 3 major variants? Where is the gene located?
    • Amyloid precurson protein
    • APP695, 751, and 770
    • Chromosome 21
  20. Functions of APP
    • Cell-cell and cell-matrix interaction
    • Cell growth
    • synaptic plasticity
    • cell surfact receptor
  21. T/F sAPP is soluble and does not form aggregates.
    True
  22. alpha secretase cleavage causes formation of sAPP alpha into the ______ space
    extracellular
  23. sAPPa regulates ____ levels and stimulates _____ _____.
    • Calcium
    • Signal transduction
  24. Intracellular domain of sAPPa acts as adaptor protein for _-protein.
    G-protein
  25. gamma secretase occurs ____ the membrane
    inside
  26. AB 1-40 and 1-42 form ____ ____.
    insoluble fibrils
  27. T/F AB 1-42 is more soluble than AB 1-40
    False, flipped
  28. T/F amyloid fibrils act as centers for deposition by other proteins.
    True
  29. AB peptides activate protein phosphorylation through this protein
    Tau
  30. T/F AB peptides are toxic to neurons
    True, direct effect
  31. T/F release of A-beta peptides are abnormal physiological events
    False, normal
  32. mutations cause an (increase/decrease) of AB (1-40/42)
    Increase
  33. Less sufficient alpha secretase causes an (increase/decrease) of AB (1-40/42)
    increase
  34. KNOW SLIDE 42!
    slide 42, or what?
  35. Presenilins 1 and 2 are membane proteins with ____ trans-membrane domains
    multiple
  36. Familial mutations is PS1 and PS2 increase gamme secretase activity leading to
    increased AB generation
  37. PS1 mutations are responsible for _%_ of early onset AD
    70%
  38. PS2 mutations make up for _%_ of early onset AD
    5%
  39. APP with downs syndrome has an (increased/decreased) APP expression which creates (more/less) AB1-40/42 and responsible for ____ formation at age 12.
    • Increased
    • More
    • Plaque
  40. Neurofibrillary tangles have microtubules with a diameter of __nm-______nm
    200-25,000
  41. Microtubule associated proteins include
    • kinesisns
    • dyneins
    • and tau
  42. Tau is found on chromosome __, it contains _ isoforms. It is important in proper neuronal axonal transport.
    • 17
    • 6
  43. Increased phosphorylation of Tau and ubiquitylation causes formation of
    Neurofibrillary tangles
  44. PHF stands for ___ ___ ____ formed by detached ____ molecules.
    • Paired helical filaments
    • Tau
  45. GSK-3B and Cylin dependent kinase 5 are causes of _____ ____.
    Hyperphosphorylating Tau
  46. T/F E4/E4 has the lowest risk for AD
    False, highest
  47. Apolipoprotein E4 is located on what chromosome?
    chromosome 19
  48. Most abundant apolipoprotein is
    E3
  49. T/F ApoE4 does affect APP expression
    False, it does NOT
  50. ApoE4 enhances _______ of AB and decreases _____ of AB.
    • aggregation
    • clearance
  51. Drugs for AD are mainly
    Acetylcholinesterase inhibitors

What would you like to do?

Home > Flashcards > Print Preview