Disorders of Memory: Case Study: Alzheimer's Disease

Question 1

What is Alzheimer’s disease?

Answer 1

Alzheimer’s disease stands as a dementing illness. It is the most common of primary dementing illnesses (causing memory loss, confusion and disorientation).

Question 2

What kind of condition is Alzhiemer’s?

Answer 2

Progressive

Question 3

What is the biggest factor with Alzheimer’s?

Answer 3

Age

Question 4

How can definite diagnosis of AD be achieved?

Answer 4

Can only be made on pathology (i.e. autopsy)

Question 5

What can only be diagnosed in life?

Answer 5

Can only diagnose Dementia of the Alzheimer type

Question 6

What is the ApoE (allele) mutation?

Answer 6

The only consistent genetic marker of increased risk of AD

Question 7

What causes rare early onset of AD?

Answer 7

Autosomal dominant cause, mutation in 3 genes; amyloid precursor protein (APP), presenilin 1 (PSEN1), presenilin 2 (PSEN2)

Question 8

What do these genes alter?

Answer 8

The production of amyloid β (Aβ) peptide, which is the principal component of senile plaques

Question 9

How does down syndrome affect risk of AD?

Answer 9

People with down syndrome are unusually prone to developing AD

Question 10

What can happen to people with preclinical AD and pathology to AD?

Answer 10

Can have sudden decompensation of AD symptoms die to a neurological injury

Question 11

How is the onset of AD?

Answer 11

Insidious, gradual deterioration

Question 12

What happens in Phase 1 of AD progress?

Answer 12

Failing memory (amnestic presentation), muddled inefficiency in activities of daily living (ADL), spatial disorientation, mood disturbance (agitated or apathetic)

Question 13

What happens in Phase 2 of AD progress?

Answer 13

More rapid progress of deterioration, intellect and personality deteriorate, focal symptoms appear (dysphasia, dyspraxia, agnosia and acalculia), disturbance of posture and gait, increased muscle tome, delusion/hallucinations

Question 14

What happens in Phase 3 of AD progress?

Answer 14

Terminal stage, profound apathy (bedridden), eventually lose neurological function, bodily wasting occurs

Question 15

What are Mckhann et al’s criteria for diagnosis for AD?

Answer 15

Probable AD, Possible AD, Definite AD

Question 16

What are the criteria for Probable AD?

Answer 16

Deficits in 2 or more areas of cognition; amnestic presentation is the most common. Progressive worsening of memory and/or other cognitive functions, no disturbance of consciousness, must be in the absence of other causes

Question 17

What happens if a person has a deficit in only one area?

Answer 17

Classified as mild cognitive impairment (MCI), AD may be developed after MCI

Question 18

What is the criteria of possible AD?

Answer 18

Made on the basis of dementia syndrome if they have variations in onset, presentation or clinical course, can be made in the presence of another disorder, which is not considered to be the cause of the dementia

Question 19

What is the criteria for definite AD?

Answer 19

Histopathological evidence of AD obtained from biopsy or autopsy

Question 20

What is the pathology of AD?

Answer 20

Grossly atrophied brain (shrunken); affects frontal and temporal lobes>parietal-occipital regions, extensive degeneration of neurons, accompanying glial cell proliferation, extensive amounts of senile plaques, extensive amount of neurofibrillary tangles

Question 21

What is the course of neuropathological changes of AD?

Answer 21

Senile plaques and neurofibrillary tangles commence in the hippocampus/MTL, then spread posteriorly to the parietal cortex, then spreads to involve the frontal cortex

Question 22

What do you see initially with AD?

Answer 22

MTL memory impairment, due to early predominance of hippocampal/MTL involvement

Question 23

How is anterograde memory affect in AD?

Answer 23

Impaired new learning, impaired delayed recall, poor recognition memory

Question 24

How is reterograde memory affected in AD?

Answer 24

Intact for remote memories, reduced for recent reterograde memories

Question 25

When is wernicke-type aphasia due to and what is it characterised by?

Answer 25

Due to spread into posterior temporal lobe, word finding difficulties, fluent grammatical speech

Question 26

What happens when AD spread into the parietal lobes?

Answer 26

Visuospatial deficits and topographical disorientation, dyspraxia, agnosia and acalcuia

Question 27

What happens when AD spreads to the frontal lobes?

Answer 27

See behaviour change, apathy and agitation

Question 28

What are treatments for AD?

Answer 28

Some pharmalogical treatment has been developed, trying to rebalance the action of acetylcholine. Best the medications can offer is longer plateau for better quality of life then sharp drop off

Question 29

What are the differences and similarities for AD and normal aging?

Answer 29

Changes that occur with AD also occur in normally aging individuals but the pathological changes are considerably greater in AD, cognitive deterioration is evident in normal aging, cognitive function in DAT is significantly impaired relative to same aged peers