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BIPN 152 > Midterm Two > Flashcards

Midterm Two Flashcards

1
Q

what are the 3 categories of brain disorders

A

neurodegenerative, psychiatric, neurodevelopmental

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2
Q

what are some examples of neurodegenerative diseases?

A

alzheimer’s, huntington’s, parkinson’s, ALS

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3
Q

Alzheimer’s is primarily _______. but some rare _______ forms have early onset (before age 65)

A

sporadic, familial

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4
Q

define Alzheimer’s

A

progressive loss of brain function due to increasing synaptic connections, degeneration of axons and dendrites, and eventual death of neurons

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5
Q

what are the two defining AD pathological lesions

A

amyloid plaques, neurofibrillary tangles

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6
Q

beta amyloid (A-Beta) has a strong tendency to fold into

A

Beta pleated sheets

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7
Q

amyloid plaques drive from

A

amyloid precursor protein

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8
Q

A-beta forms from what process

A

proteolytic processing

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9
Q

sequential cutting by what creates A-beta monomers? After, what do the monomers readily aggregate into?

A

B-secretase and gamma-secretase. oligomers

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10
Q

why does normal A-beta production not cause pathology

A

because it is continually cleared into the CSF and then the blood

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11
Q

when does a-beta become toxic

A

when it accumulates in the brain

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12
Q

early AD can occur in _______ syndrome

A

down

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13
Q

____ gene affects risk of developing AD

A

APoE

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14
Q

the APOE gene belongs to a family of lipid-binding proteins called

A

apoliproteins

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15
Q

individuals with APOE_ and APOE_ confer the HIGHEST risk of AD

A

4/4

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16
Q

the age of onset of AD is ________ on average with the APoE4 allele

A

earlier

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17
Q

extracellular plaques = excessive _______
intracellular tangles = abnormal ______

A

Abeta, tau

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18
Q

what is the abeta hypothesis

A

overproduction of Abeta is the direct and primary cause of AD

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19
Q

what is the tau hypothesis of AD

A

abnormal phosphorylation and missorting of tau is direct and primary cause of AD

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20
Q

microtubules exhibit ______ ______ in cells. alternating periods of growth and shrinkage

A

dynamic instability

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21
Q

tau is a __________-associated protein

A

microtubule. binds along microtubules to stabilize them and regulate cargo transport

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22
Q

tau binding to microtubules is regulated by

A

phosphorylation

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23
Q

in AD, tau becomes missorted to

A

dendrites

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24
Q

the number of neurofibrillary tangles is a better indicator of

A

AD severity

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25
Q

_________ is a class of neurological disease characterized by presence of tau-containing NFT

A

taupathies

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26
Q

braak stages in AD

A

progressive spread of P-tau-containing NFTs beginning in entorhinal cortex, eventually spreads to many cortical regions throughout brain

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27
Q

sporadic genetic causes of AD

A

PS1, PS2, APP

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28
Q

familial genetic cause of AD

A

APOE

29
Q

what are the three main pathological signs in the brain indicating presence of AD

A
  1. abeta plaques
  2. tau tangles
  3. reactive microglia
30
Q

_________ also plays a critical role in AD

A

neuroinflammation

31
Q

hallmarks of PD

A

loss of motor fxn
- tremor
- rigidity
- slowness, difficulty initiating movement
- posture and gait instability

32
Q

PD affects what part of brain

A

midbrain

33
Q

DA neurons in the _______ _________ in the midbrain die in PD. this leads to less DA release in the __________

A

substantia nigra, striatum

34
Q

precursor of DA

A

L-DOPA

35
Q

DA neurons in SN project to

A

striatum

36
Q

DA neurons in VTA project to

A

cortex, forebrain

37
Q

catacholamines are derived from

A

tyrosine

38
Q

what creates L-DOPA

A

tyrosine hydroxylase

39
Q

__________ is a drug often given to patients with PD

A

L-DOPA. replaces dopamine

40
Q

what is the problem of using L-DOPA as a drug

A

eventually all neurons that make DA die

41
Q

___ ____ are a characteristic pathology in PD

A

lewy bodies

42
Q

lewy bodies contain

A

misfolded aggregated fibrils of alpha-synuclein

43
Q

HD is hereditary. it is _____ __________

A

autosomal dominant

44
Q

HD occurs from degeneration of _______ neurons in the __________

A

GABAergic, striatum

45
Q

genetic basis of HD

A

expansion of CAG nucleotide repeats

46
Q

CAG encodes glutamine (Q) therefore, HD is a __________ disorder

A

PolyQ

47
Q

______ is a chronic neurodegenerative disease that affects motor neurons

A

ALS

48
Q

ALS attacks both ____ and _______ motor neurons

A

upper and lower

49
Q

most ALS cases are __________

A

sporadic

50
Q

in ALS, RNA binding protein ______ loses its normal fxn in gene regulation and forms aggregates

A

TDP-43

51
Q

limb vs bulbar onset ALS

A

limb: begins in arms or legs
bulbar: sx in speech or swallowing problems

52
Q

order of mutated genes in ALS by prevalence

A

C9orf72, SOD1, TARDBP, FUS

53
Q

nearly ALL patients have clumps of _____ in their motor neurons even without _______ mutations

A

TDP-43, TARDBP

54
Q

hemorrhagic stroke

A

burst vessels

55
Q

ischemic stroke

A

blocked vessel

56
Q

early on in a stroke, neurons die via _______ __________ (pathological cell swelling) or a form of necrotic cell death

A

cytotoxic edema

57
Q

at later times in a stroke, neurons die via _____

A

apoptosis

58
Q

core of stroke

A

area of intial damage due to low blood flow. death via cell edema. irreversible

59
Q

penumbra

A

area of cell stress and partial damage, may be rescuable if treated early. death via apoptosis

60
Q

what is ionic cause of cytotoxic edema

A

excess sodium and chloride entry, causing osmotic stress

61
Q

“Spreading depolarization” driven by _______ recruits more neurons to be damaged in a stroke

A

glutamate

62
Q

excess intracellular calcium damages ________

A

mitochondria

63
Q

penetrating TBI

A

skull fracture, gunshot

64
Q

diffuse TBI

A

blunt head trauma (sports, falls, warzone)

65
Q

concussions are considered a ____ TBI

A

mild

66
Q

repeated mild TBI causes

A

chronic traumatic encephalopathy (CTE)

67
Q

CTE is a

A

taupathy

68
Q

CTE tau tangles begin in depths of

A

sulci

69
Q
A

BIPN 152 (4 decks)

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