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Alzheimer's Disease

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Alzheimer's Disease

  1. 1. Alzheimer’s Disease Alzheimer’s is a degenerative disease of the brain, resulting in: cognitive and behavioural impairment, it interferes significantly with social and occupational functioning. It is often Medically referred to as DAT: ‘Dementia of Alzheimer’s Type’ Epidemiology:  The MOST COMMON cause of Dementia – accounts for ~70% of cases  Prevalence = 500, 000 (UK) and 30 million (Worldwide)  Risk increases with age: o 1% at 60 years o 40% at 85 years  Men and women are at equal risk, however women have a longer life span – therefore there is a higher prevalence of women with Alzheimer’s than men  Burden is likely to increase with more of the population reaching old age (>65 years) Risk Factors: Protective Factors: Pathophysiology: o Up to 50% of Neurons and Synapses in the Cortex and Hippocampus are lost o There are TWO universal hallmarks of Alzheimer’s – as identified by Alois Alzheimer in his original description of the disorder: 1. Amyloid Plaques  Insoluble B-amyloid peptide deposits as Senile Plaques  Present in: Hippocampus / Amygdala / Cerebral Cortex  ↑Density = Advanced disease 2. Neurofibrillary Tangles (NFT’s)  Phosphorylated Tau Protein  Present in: Hippocampus / Substantia Nigra / Cerebral Cortex  DDx: Down’s Syndrome; Dementia Pugilistica; Progressive Supranuclear Palsy
  2. 2. Genetics: Chromosome 21 Gene codes  Amyloid Precursor Protein (APP) - also implicated in Down’s Chromosome 19 Gene codes  Apolipoprotein E4 – alleles of which increase risk of DAT Chromosome 14 Gene codes  Presenilin 1 – Implicated in B-amyloid peptide Chromosome 1 Gene codes  Presenilin 11 – Implicated in B-amyloid peptide Cholinergic Hypothesis: o The Pathological changes above  degeneration of cholinergic nuclei in the Forebrain o This results in reduced Cortical Acetylcholine Clinically Early symptoms: ↑ Forgetfulness; deteriorating self-care; Wandering and Irritability THREE Main groups of symptoms: 1. Confusion:  Amnesia: Universal, mainly for recent events  Disorientation: Common – Person / Place / Time (Time especially)  Declining Executive Function 2. Changes in:  Personality: Often an exaggeration of its pre-morbid form with coarsening of affect and increasing egocentricity  Behaviour: Aggression, wandering, explosive temper, sexual disinhibition, incontinence, excessive eating and searching behaviour 3. Development of:  Psychiatric symptoms: o Depression is common o Delusions (15% - Usually paranoid) o Auditory and/or Visual Hallucinations (10%)  Focal Cognitive Defects: o Aphasia: Receptive and Expressive o Agnosia = Inability to recognise parts of the body o Apraxia = Awkwardness of sequence of dressing o Visual Spatial Impairment  Spastic Paraparesis: Can occur but is an unusual and late feature Investigations:  Mental State Examination (MSE): Assess Cognitive functioning  Screening: Depression and Psychosis  Physical Examination: Focal signs, reflexes, plantar responses, gait and signs of Parkinson’s Disease  Bloods: FBC, U&E’s, LFTs, TFT, Glucose, B12/Folate, MCV and Toxicology  EEG: If you need to exclude Delirium or vCJD  Brain Imaging: o CT: Cortical atrophy (>Parietal and Temporal Lobes) + Ventricular Enlargement o MRI: Atrophy of Grey Matter (Hippocampus, Amygdala, Medial Temporal lobe) o SPECT: ↓ Regional Cerebral Blood flow (Temporal, Parietal and later Frontal lobes) o PET: 20-30% ↓Oxygen and Glucose metabolism (Temporal and Parietal lobes) o MRS (Magnetic Resonance Spectroscopy) = ↓N-Acetylaspartate
  3. 3. Prognosis:  Natural History = Gradual and progressive decline, without distinguishing features  Risk factors for a poor prognosis: o Males / Young Onset (<65years) /Parietal Lobe Damage / Prominent behaviour problems / Focal deficits e.g. Apraxia / Depression / Absence of misidentification syndrome – oddly. Management  Non-Pharmacological: o Nursing Care – this can be in the community or in a residential home o Timelines – reminding patients of significant events in their lives o Timetables – reminding patients of day to day activities o Activities to improve QOL e.g. Outings / Music or Animal Therapy (!)  Pharmacological: o Acetylcholinesterase Inhibitors  1st line in Mild to Moderate Alzheimer’s (MSE >12):  Diagnosis: In a specialist clinic, according to standard diagnostic criteri  Initiated by: Old age Psychiatrists / Neruologists / Care of the Elderly Physicians, only.  Review: 2-4months after reaching maintenance dose  Follow up: 6 monthly, stop if having no benefit / MSE drops to <12  Act by enhancing Acetylcholine at Cholinergic synapses in the CNS  In this way, they may slow progression of the disease – reducing time spent in full nursing care. They have beneficial effects on:  Cognitive; Functional and Behavioural symptoms  1st Generation:  Tacrine QDS – less used as can cause Hepatoxicity  2nd Generation:  Donepezil Contraindicated in Asthma, OD  Rivastigmine BD Not Contraindicated in Asthma or COPD  Galantamine BD o NMDA Receptor Antagonist  Blocks the excessive levels of Glutamate that may lead to neuronal dysfunction  Memantine – used in moderate to severe Alzheimer’s disease  RCT’s show that memantine has a positive effects on: Cognition, Mood, Behaviour and Functioning. However there is no evidence that is slows down neurodegenration in Alzheimer’s o Others “in the pipeline”  Anti-oxidants e.g. Vitamin E and Selegiline  Anti-inflammatories e.g. NSAIDs  Amyloid Beta peptide Vaccination  Cholesterol lowering drugs e.g. Statins  Red wine (!) Key Points:  Alzheimer’s disease is the most common form of Dementia  Pathophysiology: Amyloid Plaques and Neurofibrillary Tangles  CT scan = Cortical Atrophy + Widening of Ventricles  Acetylcholinesterase Inhibitors (MSE >12) = Donepezil, Rivastigmine and Galantamine References: 1. Semple, D. Oxford Handbook of Psychiatry: 2nd Edition. Oxford University Press; 2009 2. Bourke, Castle and Cameron. Crash Course Psychiatry. 3rd Edition. Mosby Elsevier; 2008

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