Alzheimers disease is one of the most common neurological disorders accounting for 55-70% of adult-onset dementias and afflicting

g around 750k people in the UK. It was first recognized as a distinct disease by Alois Alzheimer in 1906.

Its a degenerative brain disorder, characterized by progressive intellectual and behavioural deterioration. Usually symptomatically heralded by memory problems; other symptoms include deterioration of language, mood changes and loss of initiative. The onset is >65yrs of age and typical life expectancy is around 10yrs from diagnosis, with a maximum of 20yrs [not enjoyed by some!]. So, to look at the causes - which are not fully understood. Alois Alzheimer found neuritic plaques and neurofibrillary tangles in the brain of his patient back in 1906 these are the classic pathological hallmarks of AD. But what exactly are neuritic plaques and neurofibrillary tangles? And how do they cause these symptoms? The neuritic plaques are dense, roughly spherical structures containing beta-amyloid proteins once deposited these plaques provoke an inflammatory response which results in degeneration of nearby neural cells. Amyloid proteins are coincidently implicated in a number of other diseases including Bovine spongiform encephalopathy (BSE)

Tissue from the hippocampal region of the brain is stained brown to display the tau protein. The triangular shapes are neurofibrillary tangles.

The neurofibrillary tangles resemble tiny bundles of knotted string, and are made from a protein called tau. Its not well understood what if any impact these have upon AD. Just that their number increases as the disease progresses.

So, to look quickly at risk and protective factors: The vast majority of cases do not appear to be inherited. The literature on other risk factors is unclear and sometimes contradictory. The protective factors with most evidence appear to be: mental exercise, physical exercises, modest alcohol intake, and healthy diet with high levels of antioxidants. To conclude, there are two treatment strategies: symptomatic therapies and disease-modifying therapies.

The symptomatic therapies are based on the observation made by researchers in late 1970s that levels of a neurotransmitter called acetylcholine were lower in the brains of AD patients. So the idea of using drugs to increase levels of acetylcholine was developed. This has to date proved the only moderately effective method of improving cognitive function in AD patients. The disease-modifying therapies are aimed at stopping the formation of the neuritic plaques whilst research continues into these, as of yet there have been no success.