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Brain and Behavior > Lectures 58, 60: Dementia and Alzheimer's > Flashcards

Lectures 58, 60: Dementia and Alzheimer's Flashcards

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1
Q

No pathology/abnormal cognition

A

Cognitively frail aging

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2
Q

Abundant pathology/normal cognition

A

Resilient aging

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3
Q

Cognitive changes associated with normal aging (3)

A

Mild decline in memory, impaired prefrontal fxns, decreased fine motor coordination

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4
Q

T/F: Normal aging due to neuronal death?

A

No!

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5
Q

Mild Neurocognitive Disorder

A

Modest cog decline in 1+ domains but deficits do not interfere w/ capacity for ind.

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6
Q

Mild Neurocognitive Disorder: % progress to dementia per year and % improve

A

10% progress per year; 30% improve

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7
Q

Dementia (def)

A

Clinical syndrome marked by progressive cognitive impairment in clear consciousness

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8
Q

DSM-V Major Neurocognitive Disorder Dx Criteria

A

Significant cognitive decline from a previous level of performance in 1 or more cognitive domains based on individual concern/informant and impaired performance

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9
Q

Risk factors for dementia (5)

A

Age, female, vascular, env’t, genetics

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10
Q

Resilience for dementia (9)

A

Education, social networks, cognitive stim activities, leisure activities, exercising, conscientiousness, male, statins, control vascular factors

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11
Q

Why do we care about the behavioral/psychiatric symptoms of dementia?

A

Serious burden for caregivers and institution, associated with poor outcomes

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12
Q

Three broad categories of dementia, an example of each, and symptoms

A

Cortical (AD: memory impairment, language deficits, apraxia, agnosia, and visuospatial deficits) vs Subcortical (PD: motor signs, recall, decreased verbal fluency without anomia, bradyphrenia, depressed mood, affective lability, apathy, and decreased attention/concentration) vs Mixed (Lewy body)

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13
Q

List some of the varied etiologies of dementia and give an example of each (5)

A

Primary (AD), infections (HIV), vascular/traumatic (stroke), toxic-metabolic (B12), psychiatric (schizophrenia)

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14
Q

MOST COMMON CAUSE OF DEMENTIA and %

A

Alzheimer’s Disease = 50-75%

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15
Q

Age of onset of AD

A

Typically after 65

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16
Q

AD consists of (dx criteria)…Death when?

A

Memory impairment + 1 other cognitive deficit; 8 - 10 years after sx onset

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17
Q

Describe dementia with Lewy Bodies: 3 hallmarks and one way to distinguish from AD

A
  1. Fluctuating cognition; 2. Visual hallucinations; 3. Spontaneous Parkinsoniasm; early frontal and visuospatial deficits before memory impairment
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18
Q

Vascular dementia. Dx requires?

A

Cognitive decline caused by ischemic or hemorrhagic injury to the brain; focal neurological symptoms/imaging

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19
Q

Etiology of vascular dementia (6)

A

Stroke, small vessel ischemic disease, hemorrhage, chronic hypoperfusion (i.e. lung disease), genetic conditions, cerebral amyloid angiopathy

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20
Q

Frontotemporal dementias have a proclivity for…What protein? Death?

A

Young people (onset 45-65 years old); tau-opathy; 3-5 years to death

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21
Q

Frontotemporal dementias associated with what symptoms?

A

Personality changes: disinhibition, executive dysfunction, frontal release sign, aphasia

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22
Q

Balloon or Pick cells associated with…

A

FTD

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23
Q

CJD is different from the other dementias why?

A

Very rapid (death 6-9 months from onset)

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24
Q

Reversible causes of dementia (6)

A

Normal pressure hydrocephalus, thyroid dysfunction, dietary deficiencies, infection (syphilis), depression, tumor

25
Q

ADLs are…what’s the other group called?

A

Basic (toilet); Instrumental Activities of Daily Living (IADLs)

26
Q

Describe delirium (what is it NOT and what is required?)

A

Acute, fluctuating disturbance of consciousness with reduced ability to focus, sustain or shift attention NOT better accounted for by established dementia CAUSED by a medical condition

27
Q

Everyone with delirium has…

A

Poor attention/vigilance

28
Q

Where is delirium common?

A

Hospitals

29
Q

T/F: Delirium often persists well after the precipitants have been successfully addressed and removed

A

True!

30
Q

What is a good reason to diagnose delirium quickly?

A

Late diagnoses = worse outcomes

31
Q

Description of gross and histo brain changes seen in normal aging

A

Widened sulci, larger ventricles that is greater in gray matter; loss of neurons, accumulation of lipofuscin pigment, more astrocytes, extra cellular plaques

32
Q

T/F: Can you ever see neurofibrillary tangles in normal brains?

A

True

33
Q

Four physiologic changes of normal aging

A
  1. Increased MHC antigens in brain; 2. Reduced synaptic plasticity; 3. Decreased hippocampal neurogenesis; 4. Increased BBB permeability
34
Q

In 1907, these three characteristics of AD were described

A

Dementia, extracellular AB plaques and intracellular neurofibrillary tau tangles

35
Q

Tangled tau proteins are…

A

Hyperphosphorylated

36
Q

% of AD >80 years

A

35%

37
Q

Probable Alzheimer’s disease is diagnosed if either…

A
  1. Genetic testing; 2. Clear evidence of memory decline, progressive, no evidence of mixed etiology
38
Q

What do we have AD biomarkers for?

A

Amyloid beta deposition (low CSF AB42, PET amyloid) and Downstream neuronal injury (elevated CSF tau, PET, MRI of temporal atrophy)

39
Q

Biological factors for AD

A

Genetic alterations, abnormal immune, medical problems (diabetes, HT, obesity, depression)

40
Q

Environmental factors for AD

A

Traumatic injury, drugs, smoking, low education, low physical activity

41
Q

Gross brain changes in AD

A

Cerebral cortical atrophy (frontotemporal); dilation of LVs; hippocampal atrophy

42
Q

Microscopic changes in AD (3 + 3 “other”)

A

Extracellular amyloid beta plaques; intracellular tau tangles; loss of hippocampal and cortical neurons, especially those involving diffuse cholinergic projections; other: synaptic loss, inflammation, oxidative stress

43
Q

What’s interesting about tangles?

A

Correlated with cognitive decline and length of illness (plaques are not like that)

44
Q

Describe plaques (what’s inside, what’s outside)

A

Central core of Aβ4 protein that has a beta-pleated sheet configuration often surrounded by abnormal neurites

45
Q

Genetics of AD are associated with…

A

Autosomal dominant mutations in one of three genes that are involved in amyloid protein

46
Q

What’s the most important genetic risk polymorphism factor for AD? Present in what % of AD patients? OR?

A

Abnormal ApoE gene (amyloid accumulation); 50%; 2 alleles, OR = 11

47
Q

What is the Amyloid Hypothesis? Why is this hypothesis challenged?

A

Deposition of Aβ peptides in cortex, especially Aβ42, initiates a pathogenic cascade which ultimately leads to synaptic dysfunction, neurodegeneration (tangles, cell death) and cognitive/functional decline; Plaque load (unlike tangles) does NOT predict cognitive status decline in AD

48
Q

What was the theory modification of the Amyloid Hypothesis

A

Pathological AB-oligomerization that leads to AD plaques (cannot be stained for) could be the actual problem

49
Q

T/F: It seems that AB42 is better than tau to predict AD development from minor impairment

A

False! Tau appears to be a better predictor. It is sensitive, but maybe not very specific

50
Q

Why are cortical-cortical circuits disrupted in AD? What does this disruption do?

A

Tangles and plaques thought to disrupt these circuits; breaks connection b/t association regions and hippocampus

51
Q

Evidence for cholinergic deficiency in AD

A

Degeneration of cholinergic projections; loss of cell bodies in nucleus basalis; reduced CAT (makes ACh); anticholinegic drugs –> memory problems

52
Q

AD Treatments and mechanism

A

ACHE inhib (donepezil, galantamiie, rivastigmine) and NMDA-receptor antagonist (memantine)

53
Q

Why would a NMDA-receptor antagonist work?

A

Blocks excitotoxic effects of excess glutamate at NMDA receptor

54
Q

Efficacy data for AD drugs (summary and what it does NOT do)

A

Small treatment effect sizes for cognitive function, activities of daily living and global assessment but does NOT modify disease course

55
Q

Anti-amyloid targets for AD therapy include (2)

A

Immunotherapy (vaccine) and anti-aggregants via enzyme activity

56
Q

Some other new targets for AD therapy are? (5)

A

Tau, cholinergic system, omega 3 fatty acids, inflammation, polyphenols (anti-oxidant)

57
Q

What’s a simple statement behind diet/lifestyle prevention for AD?

A

Good for heart = good for head

58
Q

How would you distinguish cortical from subcortical dementia?

A

Cortical = memory impairment includes recognition and language impairment includes anomia; Subcortical = motor involvement, affective involvement (depression, lability)

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