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BMS200 > wk 13, lec 1 > Flashcards

wk 13, lec 1 Flashcards

1
Q

dementia definition

A
  • Memory impacted most, cant perform daily activities
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2
Q

risk factors for dementia

A

o Under 45: lower education, less cognitive reserve
o Hearing loss; temporal lobe decrease in volume (hippocampus + entorhinal cortex)
o Traumatic brain injury (TBI): hyperphosphorylated tau
o Hypertension: decreased brain volume, increase white matter
o Alcohol: prolonged abstinence is bad; right sided hippocampal atrophy
o Obesity
o Smoking
o Depression
o Social isolation: social is goof for cognitive reserve
o Physical inactivity: CVD morbidity
o Air pollution: increase AB deposition and amyloid precursor protein
o Diabetes: T2D

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3
Q

pathogenesis of dementia

A

o Memory impairment: cerebrum, diencephalon and medial temporal lobes
o Impaired language: perisylvian parts of dominant frontal, temporal and parietal lobes
o Loss of reading and calculation: posterior left (dominant) cerebral hemisphere
o Loss of gestures (apraxias): dominant parietal region
o Impaired drawing: parietal lobe on non dominant (right side)
o Behaviour and personality- frontal lobe

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4
Q

degenerative types of dementia

A

o Cerebral cortex, diencephalon, basal ganglia
o Thalamus and cerebral cortex= memory
o Alzheimers damages hippocampus and cholinergic nuclei

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5
Q

inclusions in dementia

A

o Intracellular inclusions
o Disrupt normal protein homeostasis
o Stress response inclusions

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6
Q

CHART TO DIFFERENTIATE THE DISEASES

A
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7
Q

what inclusions are in Parkinson’s and dementia with Lew bodies

A

alpha synuclein

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8
Q

what inclusions are in frontotemporal dementia

A

tau

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9
Q

what inclusions in alzheimers

A

beta amyloid and tau

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10
Q

arteriosclerotic cerebrovascular disease contributing to dementia

A
  • Multiple infarcts to thalami, basal ganglia, brainstem, cerebrum  affects motor, sensory and visual
  • Recurring strokes cause multi-infarct or vascular dementia (not just the arteriosclerosis)
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11
Q

severe cerebral trauma lesions

A
  • In frontal and temporal poles, corpus callosum and thalamus
  • Disrupt white matter; axonal shearing or diffuse axonal injury
  • Chronic hydrocephalus
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12
Q

inflammatory conditions can contribute to dementia

A
  • Inflammatory and loss of neurons- syphilis, cryptococcosis, chronic meningitides, viral infections (HIV, herpes)
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13
Q

prions disease

A

widespread loss of cortical neurons, gliosis, spongiform changes

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14
Q

leukodystrophy

A

manifests as subcortical dementia; White matter lesion from advances MS, multifocal leukoencephalitis, or vascular dementias

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15
Q

how are proteins impacted in dementia

A
  • Sequester proteins and macromolecules and make them ineffective- physically obstruct axons, dendrites and movement of material in cytoplasm- disrupt homeostasis and protein recycling
  • Aggregated proteins form ultrastructural fibrils  cytotoxic
  • Revolve around proteostasis, folding and degradation of proteins…
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16
Q

what is found in alzheimers

A

beta amyloid and tau

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17
Q

who does alzheimers occur in

A
  • Most common form of dementia in elders
  • Women 2x
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18
Q

most common type of dementia in elders

A

AD

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19
Q

findings in AD

A
  • Cortical atrophy (parahippocampal region) and hydrocephalus ex vacuo
    -neuritic plaques
    -neurofibrillary tangles
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20
Q

brain changes in AD

A
  • Gyri narrow, sulci widen, ventricular enlargement, reduced brain weight
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21
Q

neuritic plaques (sensile plaques) in AD

A

o Affect gray matter, reactive astrocytes and microglia, distorted neuronal processes, beta amyloid plaques
o Quantity and distribution of plaques don’t closely algin with severity

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22
Q

neurofibrillary tangles in AD

A

o Polymerized tau filamants intracytoplasmically
o Can have these tangles in entorhinal cortex and parahippocampal gyrus and be asymptomatic, years before developing AD

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23
Q

intracellular vs extracellular changes in AD

A
  • Intracellular neurofibrillary tangles with hyperphosphorylated tau
  • Extracellular amyloid plaques with beta amyloid core (from amyloid precursor proteins, APP)
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24
Q

3 sites the amyloid precursor proteins undergo hydrolysis in AD

A

o APP undergo hydrolysis at three sites: alpha, beta and gamma secretase
 Alpha secretase produces non-toxic peptides
 Beta and gamma secretase generate toxic peptides

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25
Q

which of alpha, beta and gamma secretase; which are toxic and non-toxic

A

 Alpha secretase produces non-toxic peptides

 Beta and gamma secretase generate toxic peptides

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26
Q

which ion is impacted in AD

A
  • Toxic polypeptides aggregate extracellular and adhere to AMPA receptors and Ca2+ channels  Ca2+ influx
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27
Q

clinical features in AD

A

o Progressive memory and cognitive decline and language and behavioural alteration

o Common medical complications such as bronchopneumonia, urinary tract infections, and pressure ulcers often contribute to mortality.

28
Q

3 stages of AD

A

presymptomatic
mild cognitive impairment
AD

  1. Presymptomatic: accumulation of extracellular beta amyloid and tau tangles in hippocampus and temporal cortex; no cognitive impairment
  2. Mild cognitive impairment (MCI): not affecting ADL; low levels of CSF beta amyloid 1-42 or elevated amyloid load on PET scan
  3. AD: neurophysiological evaluation
29
Q

what are the accumulates in picks disease (frontotemporal dementia) and how does it differ from alzheimers

A
  • Accumulate tau (NOT beta amyloid- so differentiate from AD)
30
Q

what are the changes seen in picks disease (frontotemporal lobe dementia) to functioning and how does it differ than alzheimers

A
  • Also starts with disruptive and inappropriate behaviour (not memory like AD)
31
Q

causes of picks (frontotemporal dementia)

A
  • Majority are sporadic, but also 40% have hereditary component
32
Q

2nd most common cause of early onset dementia < 65 years old

A

Pick disease (frontotemporal lobe dementia; FTLD)

33
Q

knife edge atrophy in Pick disease (frontotemporal lobe dementia; FTLD)

A
  • Cortical atrophy in frontotemporal regions, reduced and thin silvers gyri
34
Q

changes in Pick disease (frontotemporal lobe dementia; FTLD)

A
  • Loss of neurons and astrogliosis
35
Q

what are picks bodies

A
  • Residual neurons are argentophilic (silver) and tau-immunoreactive round cytoplasmic inclusions = Picks bodies
36
Q

3 subtypes of Pick disease (frontotemporal lobe dementia; FTLD)

A
  1. behavioural variant
  2. Primary progressive aphasia (PPA) – semantic variation
  3. Primary progressive aphasia nonfluent/agrammatic variant
37
Q

Behavioural variant (bvFTD) of Pick disease (frontotemporal lobe dementia; FTLD)

A

 Apathy, disinhibition, impaired judgement, loss of empathy, eating disorders

 Compromised insight, compulsive behaviours, depression

38
Q

o Primary progressive aphasia (PPA) – semantic variation of Pick disease (frontotemporal lobe dementia; FTLD)

A

 Decline in capacity to comprehend words, objects, individuals, and emotions

39
Q

o Primary progressive aphasia nonfluent/agrammatic variant of Pick disease (frontotemporal lobe dementia; FTLD)

A

 Impaired motor speech and word generation
 Motor neuron disease can accompany any of the subtypes

40
Q

progression of Pick disease (frontotemporal lobe dementia; FTLD)

A

3-10 years leads to death

41
Q

2 types of lewy body dementia

A

Parkinson and dementia (PDD) or Lewy body disease (LBD)

42
Q

what do Parkinson and dementia (PDD) or Lewy body disease (LBD) both have

A

o alpha synuclein aggregates in neurons and glia= synucleopathies
o both have executive, attentional, visuospatial deficits
o episodic memory is relatively preserved
o prodromal phase of mild cognitive deficits

43
Q

what is relatively perserved in Lewy body dementia

A

episodic memory

44
Q

aggregate in Lewy body dementai

A

alpha syncline

45
Q

what is absent in Lewy body dementia

A
  • Lewy body inclusions and absence or limited # of neurofibrillary tangles and amyloid plaques
46
Q

factors for Lewy body dementia

A
  • Genetic and environmental factors
47
Q

lewy bodies

A

intraneuronal cytoplasmic inclusion of straight neurofilaments
o Bodies contain epitopes recognized by antibodies against phosphorylated and non-phosphorylated neurofilament proteins ubiquitin and alpha synuclein

48
Q

Lewy body found in

A

brainstem, substantia nigra, amygdala, cingulate gyrus, neocortex

49
Q

3 stages of Lewy body dementia

A
    1. Brainstem predominant
    1. Transitional limbic
    1. Diffuse neocortical
50
Q

what does the cholinergic deficit in Lewy body dementia cause

A

inattention, character fluctuations and visual hallucinations

51
Q

progression of Lewy body dementia vs Parkinson dementia

A

LBD- - Get motor and dementia at the same time or dementia before the motor
- Affect ADL from cognitive decline more than Parkinson’s

PD- - Motor symptoms first and then get dementia

52
Q

brain areas in parkinson

A
  • Limbic and cortical areas
53
Q

what symptoms in Parkinson’s

A
  • Non motor (constipation and hyposomnia) then anxiety, depression, REM sleep behaviour disorder, parkinsonism then dementia
54
Q

diagnose Lewy body dementia

A
  • Diagnosis: Psychosis, visual hallucinations, REM sleep disorder, parkinsonism
55
Q

early sign of Lewy body dementia

A
  • REM sleep behaviour disorder is often prodromal (early sign)
56
Q

which dementia do you get - Anosmia (loose smell)

A

Lewy body dementia

57
Q

what must occur to have vascular dementia

A
  • 1+ symptomatic strokes
  • Asymptomatic vascular lesions
58
Q

stroke impact on cognition

A
  • ½ stroke survivors have cognitive impairment
59
Q

large vs small cerebral strokes and vessel disease

A
  • Large cerebral strokes
    o Symptomatic strokes, ischemic or hemorrhagic damage the cerebral cortex, white matter, and infratentorial structures
  • Cerebral small vessel disease
    o Lack of symptoms
    o Arteriosclerosis and cerebral amyloid angiopathy (beta amyloid plaques on walls)
60
Q

vascular dementia influence on concurrent brain pathologies

A

o BBB compromised; infiltrate neurotoxic or inflammatory agents

61
Q

hearing impairment and dementia

A
  • Sensorineural hearing loss in elders
  • Mild cognitive impairment and AD
62
Q

4 theories of hearing impairment and dementia

A

o Increased cognitive load (more effort to process speech)
o Changes in brain structure and function (decrease brain volume and primary auditory cerebral cortex)
o Common pathological conditions; degenerate stria vascularis, lose hair cells, primary afferent neurons
o Social disengagement and isolation

63
Q

traumatic brain injury and dementia

A
  • Cerebrovascular dysfunction
64
Q

gut microbiome and dementia

A
  • Obesity, diabetes, cancer, autoimmune, depression
  • Beta amyloid, tau phosphorylation, neuroinflammation, neurotransmitter dysregulation, oxidative stress
65
Q

Which of the following neurodegenerative diseases is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain?
- A) Vascular dementia
B) Lewy body dementia
C) Frontotemporal dementia
D) Alzheimer’s disease

A

D) Alzheimer’s disease

66
Q

Which type of dementia is associated with motor symptoms such as tremors, rigidity, and bradykinesia?
- A) Alzheimer’s disease
B) Vascular dementia
C) Lewy body dementia
D) Parkinson’s dementia

A

D) Parkinson’s dementia

67
Q

Which type of dementia is associated with a gradual decline in cognitive function due to multiple small strokes or impaired blood flow to the brain?
A) Alzheimer’s disease
B) Vascular dementia
C) Lewy body dementia
D) Frontotemporal dementia
E) Parkinson’s dementia

A

B) Vascular dementia

BMS200 (46 decks)

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