Aging and Dementia Flashcards

1
Q

What are some COGNITIVE CHANGES of Normal Aging?

A
  • Decreased Speed
  • Some diminishment of recent memory and learning
  • Decreased performance in some “frontal” tasks (ex. fluency, memory for recency)
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2
Q

What are some BRAIN CHANGES of Normal aging?

A
  • Brain weight decreases due to white matter loss**
  • Gyrus atrophy, enlarged ventricles**
  • loss of cells in the hippocampus and cortex**
  • Decreased glucose metabolism and blood flow in prefrontal cortex
  • fMRI “recruitment” of more widespread areas of the brain
  • Default mode network changes (during resting state and during task performance)

**related brain changes associated with Alzeihmer’s

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3
Q

What is a variability in the rate of cognitive loss?

A

Those with higher cognitive performance have a later onset of aging symptoms.

The rate of cognitive loss is the same but there are different levels of cognitive levels that one may start off.

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4
Q

What is Dementia in general?

A

An irreversible, progressive loss in mental functioning.

ex. memory, intellectual functions, and personality.

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5
Q

What are two types of subcortical dementias?

A

Huntington’s Disease

Parkinson’s Disease

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6
Q

What type of dementia is considered a MIXED (cortical and subcortical)?

A

Multi-infarct (vascular) Dementia

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7
Q

What are three types of Cortical Dementias?

A
  • Pick’s Disease
  • Creutzfeld Jakob Disease
  • Alzheimer’s Disease
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8
Q

What is Multi-Infarct Dementia?

A

Sudden onset, step-wise progression

Focal symptoms, may involve sensory and motor functions

Often includes Executive Dysfunctions

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9
Q

What is Pick’s Disease?

A

FRONTO-TEMPORAL DEMENTIA

Early personality or social behavior symptoms

Impairment of frontal “executive” functions

Memory Perceived in early stages

No loss of topographic sense

Speech and language symptoms

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10
Q

What is Creutzfeldt-Jakob Disease?

A

Transmissible Dementia due to “slow virus”

VERY RAPID decline in mental functions

Initial symptoms: Involuntary, movements, fatigue

Motor dysfunctions and “cognitive collapse”

Widespread neuronal loss- “spongy brain”

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11
Q

What is Alzheimer’s Disease?

A

INSIDIOUS onset of memory and high cognitive symptoms

Initial sparing of personality and social judgement

Precursor: MCI (mild cognitive impairment)

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12
Q

In Alzheimer’s what are some GRADUAL, Constant Deteriorations?

A

DECLINE SEEN IN THE FOLLOWING:

  • longterm memory (AA & RA)
  • visuospatial and topographic skills
  • Selective attention (can’t disengage attention)
  • language (first word retrieval, later comprehension)
  • Judgment, insight
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13
Q

What are some symptoms to the later stages of Alzheimer’s

A
  • hallucionation, delusions
  • profound memory and cognitive loss
  • beddridden
  • Need for constant care
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14
Q

What are some Alzheimer’s brain changes in a EGG scan?

A

Posterior slowing

reduced anterior-posterior coherence

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15
Q

What are some Alzheimer’s changes in CAT/MRI scans?

A

increased ventricle size

enlarged sulci

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16
Q

How is the correlation between brain atrophy and mental state in Alzheimer’s?

A

Poor

17
Q

What are some metabolic changes of Alzheimer’s?

A

Decreased glucose metabolism.
Earliest and most severe in parietal or parietal-temporal cortex

Decreased blood flow in temporal-parietal cortex
(unlike normal aging)

Loss of neurons of lower functioning of remaining neurons?

Task-dependent increases in activation involve more brain regions than normal

18
Q

How are COPYING TASK in Alzheimer’s patients affected?

A

Patients with primarily word-finiding deficits show FINE copying skills

Patients with primary visuospatial and constructional deficits is POOR

19
Q

What are the alterations in the default mode network seen in Alzheimer’s

A
  • Active during tasks
  • less active during passive condition
  • reduced functional connectivity within default mode network
20
Q

What are some cellular brain changes associated with Alzheimer’s?

A

Loss of neurons in forebrain (assoc cortex, hippocampus, amygdala)

loss of neurons in the nucleus basalis (normally release acetylcholine)

21
Q

What are some neuronal abnormalities associated with Alzheimer’s

A

Neurofibrillary Tangles
(density correlates with dementia)

Amyloid Plaques
Accumulation of amyloid in blood vessel

22
Q

What are possible contributors to Alzheimer’s Disease?

A

-Genetic Trait as a risk factor

Early Onset

  • # 21 amyloid precursor gene
  • # 14 presenelin 1 gene
  • # 01 presenelin 2 gene

Late Onset

  • APOE4 “predisposes” development
  • APOE normally clears amyloid plaque
  • Associated with faster hippocampal atrophy, more amyloid plaques
23
Q

What is mechanism of cognitive reserve associated with Alzheimer’s

A
  • Neural Reserve
  • Neural Compensation
  • Many factors contribute to preservation/loss of compensatory mechanisms.
24
Q

What is meant by Neural Reserve

A

Neural networks more efficient or have greater capacity

25
Q

What is meant by neural compensation

A

Greater/better use of compensatory mechanisms

26
Q

How does frequent cognitive activity relate to Alzheimer’s?

A

Later onset of Alzheimer’s Disease

More rapid decline post-onset

27
Q

Why does frequent cognitive stimulation reduce risk of Alzheimer’s?

A

Cognitively active persons start old age with higher level of function–takes longer to reach dementia stage?

Is reduced cog activity an early sign?

Slower rate of decline in those who are cognitively active?

28
Q

How is cognitive stimulation is correlated to Alzheimer’s neuropathology?

A

Less neuropathology in frequent cognitive stimulation?

Cognitive stimulation maintain neural networks, so pathological changes produce less cognitive loss-“cognitive reserve”

29
Q

What can possibly reduce risk of developing Alzheimer’s?

A

High levels of cognitive activity and/or education are associated with less risk.

Frequency of stimulating cognitive activities

Cognitive activity reduces declines in working memory and perceptual speed

30
Q

What are some other general possible contributors to alzheimer’s

A
  • Abnormal Protein (amyloid)
  • Reduced Cerebral Blood Flow
  • Acetylcholine loss
31
Q

What is the relation between Down’s Syndrome Patients and Alzheimer’s

A

By age 35: plaques and tangles in neocortex, hippocampus, amygdala

20-30% show clinical dementia

Reduced metabolism in temporo-parietal cortex

Extra set of genes on chromosome 21