Dementia
Definition and Possible Aetiologies of Dementia
Dementia
An acquired decline in intellectual function resulting in a loss of social independence
Characterised by impairment of memory and at least one other area of cortical functions, such as:
Language
Calculating
Decision making
Judgement
Spatial orientation
Abstract reasoning
As opposed to confusional states, (i) symptoms progress over months to years, and (ii) alertness is preserved until the very late stages of disease
Although it affects 5-20% of persons over 65 years, it is not part of normal ageing
When dementia is diagnosed with no antecedent cause…
Alzheimer's disease (50% of all dementia cases)
Major causes of dementia
Cerebrovascular disease and multiple strokes
Prion disease
Parkinson's disease
Alcoholism
Neoplasms
Chronic meningitis
Huntington's disease
Vitamin deficiencies (e.g., B1 and B12)
Hypothyroidism
Alzheimer's disease: Introduction and Clinical Manifestations
At age of 65 years: 5% -> at the age of 95 years: >90%
Alzheimer's disease has slow onset, usually develops over 5-10 years, and first impacts learning and recent memory
Earliest signs and symptoms
Spatial orientation -> pts get lost
Aphasia
Anomia (i.e., inability to recall names)
Acalculia
Frontal lobe gait disorder with short, shuffling steps and a tendency to fall backwards
Later stages
Personality changes
Paranoia
Hallucinations and delusions
End stage
Pts are bedridden, mute, and incontinent
Brain areas affected the most by Alzheimer's disease
Frontal lobe (prefrontal cortex)
Intelligence, judgement, and behaviour
Determine personality, character, intelligence, behaviour, and judgement
Temporal lobe
Memory
Parietal lobe
Language
Amygdala
Needed to perceive emotions and to control aggression
Hippocampus
Required for converting short-term memories to long-term memories
Alzheimer's disease: Pathogenesis
Amyloid beta-peptide accumulates as the consequence of improper degradation of a physiologically present protein (i.e., beta-amyloid precursor protein (APP))
APP is improperly cleaved, which results in the production of beta-amyloid protein (amyloid beta-peptide)
Amyloid beta-peptide is water-insoluble
Amyloid beta-peptide proteins accumulate in the extracellular space and aggregate
Amyloid plaques are formed
Amyloid beta-plaques interfere with synaptic transmission and cause neurodegeneration
Tau pathology
Healthy tau protein stabilises microtubules that are essential for axonal transport
In Alzheimer's disease, tau is dysfunctional and accumulates in the cytoplasm (even in the cell body where it is not supposed to be)
Neurofibrillary tangles
Neuronal destruction
Abnormal tau proteins accumulate intracellularly and appear ass neurofibrillary tangles
Alzheimer's disease is progressive and irreversible
Amyloid beta-plaque formation and depositions start about 30 years before the onset of mild cognitive impairment
Alzheimer's disease: Management
Prefrontal cortex, hippocampus, and amygdala
The loss of cholinergic neurons in the hippocampus and prefrontal cortex is thought to underlie the cognitive deficit and loss of short-term memory that occur in AD
In AD, there is a decrease of acetylcholine in relevant neuronal circuits
Acetylcholine gets degraded by an enzyme called acetylcholinesterase (AChE)
By inhibiting acetylcholinesterase, we can boost acetylcholine levels and prolong its effects in cholinergic synapses
Inhibition of acetylcholinesterase
Acetylcholinesterase inhibitors detectably improve cognitive impairment in clinical trials but have significant adverse effects and are of limited use clinically
They have not been shown to restart neurodegeneration
Some NSAIDS reduce the likelihood of developing AD
If you don't use it, you lose it… (synaptic pruning)
Keep your brain sharp (learn languages, engage with cross-words, and learn for the sake of learning, etc.) + healthy lifestyle