Dementia Flashcards
Most decline skill
Speed processing (digit symbol, letter, patten comparison) Working memory (reading, computation, etc) Long term memory
Last to decline
World knowledge (vocab)
What is dementia?
Declines in cognitive, function, and behaviour?
Most common cause of dementia?
Alzheimers
Cause of Alzheimers Disease?
Unknown.
Risk factor is age.
Life expentancy of A.D.
3-20yrs post diagnose.
8yrs average
Diagnosis of A.D.
History taking. Cognitive Ax (mini mental, etc) Neurological Ax Meds review Blood tests. Amyloid imaging.
Symptoms of A.D.
Changes in memory.
Atrophy of brain.
Declining amyloid-beta protein.
Atrophy of brain
Widening of sulci and enlargement of ventricles.
Most affected lobes in brain atrophy
Frontal, temporal, and parietal.
Pre clinical A.D.
First noticed in Entorhinal cortex, then proceed to hippocampus.
First sign of A.D.
Memory loss (misplace item, forget recent events, get lost easily)
Mild to moderate A.D.
Cerebral cortex begins to shrink
Mild AD signs
memory loss, confusion, trouble handling money, mood changes, increased anxiety.
Moderate AD signs
increase memory loss, problems recognising people, difficulty with language and thoughts, restlessness, agitation, wandering, etc
Sundowning behaviour
behavioural problems tend to begin or worsen in late PM/evening.
Severe AD
Extreme shrinkage in brain occur. Dependant on others for care.
Severe AD signs
weight loss, seizure, skin infection, groaning, moaning, grunting, incontinence.
Death in AD is commonly due to
Aspiration pneumonia, or other infections.
? Hypothesis of AD
Reduced choline uptake and acetylcholine release.
Loss of cholinergic neurons from basal forebrain.
Enzyme responsible for synthesis of acethycholine?
Choline acetyltransferase.
Treatment for AD
Acetylcholinesterase inhibitors.
Pathology of AD
Increased levels of amyloid beta peptide.
Increased levels of hyperphosphory-lated tau (p-tau).
Widespread loss of neurons and synapses.
What is p-tau??
a microtubule assembly protein that accumulates intracellularly as neurofibrillary tangles (NFTs).
Non AD pathway
Alpha cleavage to gamma cleavage
AD pathway
Beta cleavage to gamma cleavage.
What happens when APP is cleaved by B and Y secretase enzymes??
neurotoxic AB peptides are released.
Accumulation of AB can lead to
Axonal damage.
Synaptic damage, excitotoxicity, mitochondrial dysfunction, lysosomal failure, damage to signalling pathways.
