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Neuro > Alzheimer's > Flashcards

Alzheimer's Flashcards

1
Q

How is dementia classified?

A

major neurocognitive disorder (major NCD), based on DSM 5

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2
Q

What percentage of dementia diagnoses Alzheimer’s?

A

60-80%

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3
Q

How is one diagnosed with dementia?

A

Decline in memory and learning and at least one other cognitive domain:
complex attention, executive function, language, motor, social cognition. Must have no evidence of mixed etiology (side effects from a drug), or other medical problems, decline must interfere with daily life

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4
Q

How are you diagnosed with MILD NCD?

A

modest decline in cognitive performance in one or more of the categories, but not a sever enough decline to affect everyday life

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5
Q

Early symptoms of AD

A

difficulties w/ name recall and event recall

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6
Q

later symptoms of major NCD

A

1) confusion, impaired judgment
2) disorientation
3) general behavior changes
4) difficulty swallowing and speaking

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7
Q

brain abnormalities found

A

1) plaques- beta fragments that become sticky and clump
2) tangles- strands of tau that accumulate in neurons and kills neuron

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8
Q

Death expectancy once diagnosed

A

live an average of 8 years after diagnosis

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9
Q

What is Amnestic Mild Cognitive Impairment (MCI)?

A

occurs in very early stages of AD, display of more memory problems than the “typical” for that age group: occasional short term memory failure, some decline in word finding, impaired reasoning skills, daily activity not significantly impacted

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10
Q

What makes up the diencephalon?

A

thalamus and hypothalamus

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11
Q

what makes up the brainstem?

A

midbrain, pons (rounded), medulla (leads to spinal cord)

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12
Q

gyrus

A

a ridge of the cortex

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13
Q

suclus

A

depression in the surface of the cortex

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14
Q

what are the 5 lobes?

A

frontal, parietal, occipital, temporal, limbic (know location)

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15
Q

4 sulci?

A

central, lateral, parietooccipital, cingulate (know location)

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16
Q

What are the areas of the cerebral cortex and what are their functions/location?

A

primary motor cortex- pre central gyrus
premotor cortex- anterior to primary motor, movement planning, sensory guidance of movement
supplementary motor cortex- medial surface anterior to primary motor cortex, postural stabilization, coordinates movement between body sides

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17
Q

what is the corticospinal tract?

A

descending pathway, voluntary motor control of limbs/trunk, look at slide

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18
Q

what are the primary sensory areas and their location?

A

somatosensory- postcentral gyrus in parietal lobe, receives sensory info from periphery (temp, touch, pain)
vision- banks of calcarine sulcus in occipital lobe
auditory- transverse temporal gyrus

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19
Q

Broca’s area

A

language production, inferior frontal gyrus in dominant hemisphere

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20
Q

wernickes area

A

language comprehension, posterior part of the superior temporal gyrus and inferior parietal lobule in dominant hemisphere

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21
Q

what is arcuate fasciculus?

A

connects brooks and wernickes, axons leave one area and terminates in the other area

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22
Q

the prefrontal cortex (PFC)

A

large area, works with amygdala and hypo campus, regulates emotions and executive functions, connects to sensory areas (vision, hearing and somatosensory)

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23
Q

what does the PFC divide into?

A

dorsolateral cortex- connections with vision, hearing and somatosensory, works memory, motor planning, and organization
ventrolateral cortex- interacts w/ brain regions involved in regulating emotion, impulsitvity and self-control

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24
Q

what are the structures of the limbic system?

A

1) cingulate gryus
2) pariahippocampal gyrus
3) hippocampus
4) amygdala
5) septal nuclei

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25
Q

where Is the hippocampus and what is the function

A

location- temporal lobe
function- formation of new memories, emotion, spatial orientation

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26
Q

location and function of amygdala

A

location- medical temporal lobe, anterior to hippocampus
function- processing and memory of emotional reactions, especially fear

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27
Q

why do we vividly remember emotional experiences?

A

amygdala is closely related to hippocampus which help form memories that are connected to emotion

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28
Q

entorhinal cortex

A

part of pariahippocampal gyrus (main input region), inputs directly to amygdala, filters what makes it to the hippo.

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29
Q

what is white matter?

A

myelinated axons

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30
Q

APP

A

concentrated in synapses, aids in neuron growth and development

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31
Q

sAPPa(alpha)

A

neuroprotective properties, promotes neurotic expansion, synapse production and cell adhesion

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32
Q

AICD

A

regulates cell death, maintaining cellular actin

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33
Q

P3

A

no known function but doesn’t appear toxic

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34
Q

what are plaques surrounded by?

A

microglia and astrocytes

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35
Q

what does tau do?

A

binds and stabilizes microtubules

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36
Q

tau in AD

A

abnormal hyperphosphorylation

37
Q

what does kinase do?

A

adds phosphate group during phosphorylation

38
Q

what does phosphatases do?

A

remove phosphates

39
Q

where are tangles first observed?

A

in the entorhinal cortex

40
Q

early onset familial AD (EOAD)

A

diagnosed at <65 years old

41
Q

late onset AD (LOAD)

A

diagnosed at >65 years old, linked to genes and environment

42
Q

what’s autosomal dominance?

A

only 1 copy needed of a mutated gene to cause disease

43
Q

what is Presenilin?

A

a subunit of gamma secretase (enzyme that cuts the bottom of the amyloid protein)

44
Q

what does apolipoprotein E do?

A

transports lipids and regulates neurite outgrowth

45
Q

types of cholinesterase inhibitors?

A

1) donepezil (aricept)- for all stages
2) rivastigmine (exelon)- for mild to moderate stages
3) galantamine (razadyne)- for mild to moderate

46
Q

what does mematine (Namenda) do?

A

regulates glutamate activity

47
Q

what is ACH?

A

a neurotransmitter, widely located in the brain, stimulates learning and memory (hippocampus/cortex) and attention (cortex), also found in nucleus of meynert, septal nucleus

48
Q

what is the main input region of ACH?

A

entorhinal cortex

49
Q

what ACH enzyme is involved in synthesis?

A

cholineacteyltransferase

50
Q

What ACH enzyme is involved in metabolism?

A

acetylcholinesterase

51
Q

What does neuron degeneration result in?

A

60-80% loss of choline acetlytransferase

52
Q

what does a decrease in ACH lead to?

A

a reduction in mental capacity and learning

53
Q

what is glutamate?

A

predominant excitatory neurotransmitter, central to hippocampal learning and memory processes

54
Q

types of glutamate receptors?

A

AMPA, Kainate, NMDA, mGluR

55
Q

what is excitotoxicity?

A

triggers neuron cell death

56
Q

what do cholinesterase inhibitors do patients?

A

6-12 month duration, significant benefits for cognition usually in earlier stages

57
Q

what does NMDA receptor antagonist-memantine do for patients?

A

significant benefits in cognition and neuropsychiatric symptoms for later stages

58
Q

what does vitamin E do for patients?

A

can interact w/ cholesterol and clotting drugs

59
Q

what does gingko biloba do for patients?

A

moderate benefits but doesn’t really slow memory decline

60
Q

what does Aducanumab do?

A

recently FDA approved, appears effective in reducing amyloid plagues in mild to moderate AD, has an antibody that targets beta amyloid

61
Q

what does Lacanemab do for patients?

A

approved in 2023, works like Aducanumab but binds more tightly and stays attached to the plaques longer which reduces the plagues in MCI and mild AD

62
Q

what does Tau aggregation inhibitors do for a patient?

A

accumulates in the brain so It crosses the BBB, proteosomal degredation of tau (breaks down proteins that aren’t functioning properly), prevention of disulfide bridges from forming between tau proteins

63
Q

when do brain changes begin?

A

about 10 years before symptoms begin

64
Q

what could blood biomarkers do?

A

detect AD before cognitive symptoms appear

65
Q

what does an AD medical evaluation require?

A

medical history
mental status testing
physical and neuroscience exam
tests to rule out other dementia like symptoms

66
Q

commonly used neuropsychological testing for AD?

A

mini-mental state exam (MMSE)
mini-cog test

67
Q

what is SV-MMSE?

A

most common, for cognitive decline, 30pt test that lasts 25 min.

68
Q

what is BV-MMSE?

A

16pt test, for screening large populations/individuals, usually for a survey/study, not for cognitive complaints

69
Q

what is EV-MMSE?

A

90pt test, increased sensitivity for individuals w’/ less severe cognitive impairment, 20 min, very difficult

70
Q

what is the mini-cog test?

A

3 min test, 85-99% accuracy in predicting dementia, less influenced by education
name 3 unrelated words, patient repeats words, then draws a clock, then recalls words

71
Q

what is GPCOG?

A

General Practitioner Assessment of Cognition, similar accuracy as the MMSE
1) cognitive test
2) informant interview

72
Q

other health related problems that cause dementia-like symptoms?

A

drug interactions
iron deficiency
excessive alcohol consumption
thyroid and kidney problems

73
Q

what does an MRI show with AD?

A

brain structure, tissue loss in hippocampus and entorhinal cortex, best biomarker for AD, episodic memory loss is well correlated w/ hippocampal volumes

74
Q

what does an fMRI show for AD?

A

reveals decreased task-associated activation of parahippocampla and hippocampal regions, abnormal prefrontal activation patterns

75
Q

Pet scanning

A

shows levels of amyloid beta binding

76
Q

what compounds are used in PET scanning?

A

11C PIB, 18F florbetapir (Amyvid), 18F flutemetamol (vizamyl)

77
Q

causes of vascular dementia

A

10% of dementia cases, blood vessel blockage/damage leading to strokes or bleeding in brain

78
Q

Vasulcar dementia symptoms

A

impaired judgment or ability to make decisions, plan/ organize, symptoms appear instantly

79
Q

cause of dementia w/ levy bodies

A

build up of lower bodies in motor and cognitive areas, mainly found in Parkinson’s

80
Q

how do levy bodies form?

A

alpha synuclein sticks and bundles which forms the Lewy body in a neuron

81
Q

symptoms of lewy body dementia

A

memory loss and thinking problems, sleep disturbances, hallucinations, gait imbalance

82
Q

how to diagnose DLB?

A

dementia first, then , motor symptoms

83
Q

cause of FTD?

A

progressive nerve cell loss in frontal and temporal lobe, some have a genetic link, asymmetrical tissue loss

84
Q

3 subtypes of FTD?

A

behavior variant FTD
primary progressive aphasia
distrubances of motor function

85
Q

symptoms of behavior variant dementia

A

changes in personality, interpersonal relationships and conduct, around age 50-60, most common

86
Q

primary progressive aphasia

A

affects language skills, speaking, writing, and comprehension, diagnosed before age 65

87
Q

diagnoses of FTD

A

neurological exam, MRI/PET scans

88
Q

differences between FTD and AD

A

age of diagnosis, memory loss is an early symptom of AD, behavioral changes in bvFTD, speech problems common in PPA

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