How we change what others think, feel, believe and do
Alzheimer's Disease (often abbreviated as AD) is the leading cause of dementia.
The microscopic structure of Alzheimer’s disease has been related to both numbers and locations of senile plaques (SPs, also known as amyloid plaques, APs) and neurofibrillary tangles (NFTs) in the neo-cortex. NFTs are mostly made up of tau(t )protein.
Plaques are aggregated proteins and peptides.
Beta-amyloid is created from the beta-amyloid precursor protein (APP), which is a long chain of about 700 amino acids. This is cut at one end by beta-secretase and at the other by gamma secretase, resulting in an amyloid-beta molecule of 40 or 42 amino acids, depending on where the gamma secretase cut is placed. Normal brains have around 5-10 percent of the longer molecule. In Alzheimer's this rises to as much as 40%. High concentrations of the longer molecule do not fold properly and damage the cell. The body can cope with the normal concentration of longer molecules but gets overwhelmed by the Alzheimer's quantity. Excessive amounts of beta-amyloid in the in cell cytoplasm then causes neural degeneration.
NFTs are made up of dying neurons that contain twisted filaments of hyperphospherated tau proteins. During progression of the disease excessive amounts of phosphate ions get attached to tau protein strands, changing the molecular structure. This is seen in the soma and dendrites of pyramidal neurons in the cerebral cortex. Mutations in APP also produce tau proteins.
It may be questioned as to whether Alzheimer's is a unique disease or a collective of some sort. It has been suggested that it is changes only in the hippocampus that differentiate Alzheimer's from normal aging. The pathophysiology of this illness has been associated with a variety of factors, including the deposition of beta-amyloid plaques, accumulation of intracellular neurofibrillary tangles, oxidative neuronal damage and inflammatory cascades. More recently it is believed that the A-beta peptide, which is derived from the processing of the amyloid precursor protein (APP), is the principal agent responsible for the pathogenesis of Alzheimer’s.
In some rare instances of inherited forms of Alzheimer’s, gene mutations give rise to a beta-amyloid precursor protein which can speed symptoms. This protein also appears in Downs Syndrome and may contribute to aging.
The chance of getting Alzheimer's doubles every 5 years after the age of 65 and is about 50% at the age of 85.
Alzheimer's creates the following problems
Episodic memory is of life events, including where and when they happened.
Procedural memory is largely unaffected and sufferers can still do most jobs, although cognitive activities such as typing may be affected.
Combining two tasks
Alzheimer affects the central executive and sufferers find it difficult to do two things at once, such as walking and talking.
The condition was first identified by the German doctor Alois Alzheimer in 1906.
Alzheimer's is such a complex and varied condition it has provoked much debate, including whether Alzheimer's is just a facet of normal aging and whether it is not so much a condition as a continuum, with many of us falling beneath the radar of 'full' Alzheimer's yet still silently suffering some of the symptoms.
It can be heartbreaking for carers who may see a the personality of loved one disintegrate as they become a literal stranger.
The major response to Alzheimer's is care and teaching the sufferer coping techniques. With an aging population this is a huge and increasing cost on public (and private) healthcare.
Much money and effort is being put into the search for a cure. If a drug company finds a cure, then they will have a vast market to serve (and profit from). The best so far seem to hold back the tide for a while but little more. And the chance of repairing the widespread damage done is extremely low.