1. DEGENERATIVE DISEASES is a disease in which the function or structure of the affected tissues or organs will progressively deteriorate over time, whether due to normal bodily wear or lifestyle choices such as exercise or eating habitstissuesorgansexercise 5% of the population over 65 years of age suffer from a dementing illness. Over the age of 80, this rises to over 20%. Alzheimer's disease Parkinson's Disease Multiple system atrophy Niemann Pick disease Atherosclerosis Progressive supranuclear palsy Essential tremor Amyotrophic Lateral Sclerosis

2. ALZHEIMER'S DISEASE : the most common cause of dementia, patients over 45 years. 15% of cases are familial Familial = two main groups: 1.an early- onset, autosomal dominant pattern, 2. a later-onset group whose inheritance is not so clear.. The inheritance of one of the alleles of apolipoprotein, is associated with an increased risk of developing the disease (2-4 times in heterozygotes and 6-8 times in homozygotes). The cause of AD is unknown. Several investigators now believe that converging environmental and genetic risk factors trigger a pathophysiologic cascade that, over decades, leads to Alzheimer pathology and dementia.

3. Macroscopically, the brain is atrophic, particularly the cerebral cortex and hippocampus Histochemical staining demonstrates significant quantities of amyloid in plaques Many different neurotransmitter abnormalities have been described, in particular impairment of cholinergic transmission, although nor adrenaline, 5-HT, glutamate and substance P are also involved

4. Tau Neurofibrillary tangles (NFTs) abnormal tau tangled together results in the disintegration of microtubules which may result first in malfunctions in communication between neurons and later in the death of the cells.  senile plaques (SPs; also known as beta- amyloid plaques)  The hippocampus and medial temporal lobe are the initial sites of tangle deposition and atrophy A special kind of protein, Tau, that binds to the microtubules which forms the neuronal internal supporting structure that stabilizes them

7. Clinical manifestation 1.Gradual memory loss 2.Decline in ability to perform routine tasks 3.Disorientation 4.Loss in language skills 5.Impairment of judgment 6.Personality changes imaging studies for ruling out potentially treatable causes of progressive cognitive decline, such as chronic subdural hematoma or normal- pressure hydrocephalus. [ In patients with AD, brain MRIs or CT scans can show diffuse cortical and/or cerebral atrophy, but these findings are not diagnostic of AD

8. Treatment anticholinesterases such as Donepezil, Rivastigmine and Galantamine, and the NMDA receptor antagonist, Memantine, have been shown to be of some benefit The time from diagnosis to death varies from as little as 3 years to as long as 10 or more years. Patients with early- onset AD tend to have a more aggressive, rapid course than those with late-onset AD. The primary cause of death is intercurrent illness, such as pneumonia.

9. Wernicke-Korsakoff disease Deficiency of thiamin (vitamin B 1 )  Symptoms of Wernicke's encephalopathy 1.acute confusional state (Wernicke's encephalopathy) 2.Ataxia 3.nystagmus and extraocular muscle weakness, particularly lateral rectus weakness  Symptoms of Korsakoff syndrome: 1.dementia characterised by a profound disturbance of short-term memory 2. a tendency to confabulate Treatment consists of intravenous thiamin

10. Pick's disease degeneration predominantly affects frontal and temporal lobes personality change due to frontal lobe involvement progressive aphasia. Memory is relatively preserved in the early stages. There is no specific treatment

11. Lewy body dementia Lewy body found in the cerebral cortex cognitive impairment in the context of an extrapyramidal syndrome the cognitive features may be indistinguishable from those of Alzheimer's disease. Patients' cognitive state often fluctuates they have a high incidence of visual hallucinations particularly sensitive to the side-effects of anti- parkinsonian medication and also to neuroleptic medication there may be clinical benefit with anticholinesterase agents such as Rivastigmine