AD patients

All the AD sufferers will be male as well from this particular scenario. From autopsies and other tests on AD patients it has been discovered that the cerebral cortex is very abnormal. The cerebral cortex is involved in high order thinking such as memory, thinking and planning, so the degeneration of these functions leads to the idea that AD affects the cerebral cortex. Some of the neurones had bundles of fibres called tangles, in between the neurones were deposits known as plaques.

These cannot be seen with any scans available whilst the patient is alive although CAT and MRI scans show a reduction in the size of the brain shown left. It is not known however if these tangles and plaques result in the symptoms of AD or what makes them. The tangles are made of a protein called tau, the neurons die as that builds up. The plaques are made up of a peptide known as beta amyloid, A?. This peptide is made from a larger protein molecule called the beta amyloid precursor protein, APP which is found in plasma membranes. A protein cuts the part of the APP chain that lies outside of the membrane. The A is usually released into the tissue fluid. It has been discovered that the plaques of A? form when more A? is secreted than normal or a 42 amino acid chain is apparent in the plaques instead of 40.

This leads to the assumption that abnormal metabolism of APP is to blame for AD. Other evidence for gene involvement is the gene that codes for a protein known as APOe. Approximately half the people with AD seem to have a particular allele of a gene called e4 that codes for the protein. There is some evidence that suggests the presence of the e4 could cause the the rate of the Ab deposited on the plaques to increase. However it is not known how either of these two genetic conditions could have an effect on plaque development. However the recent discovery of Chromosome 12 mutation could have a bearing on the situation.

Scientists have become familiar with a protein known as the A2M protein found on chromosome 12. A2M is a protease inhibitor that controls the activity of enzymes that breakdown other proteins and is known to interact with a nerve cell receptor known as LRP( low-density lipoprotein receptor-related protein). There were two clues that could link mutations of A2M with AD. Firstly the two proteins Ab and APOe also interact with LRP. The second clue is that A2M tightly binds the protein fragment Beta amyloid, which is found in the plaques found in the cerebral cortex.

A2M facilitates the removal of Beta amyloid from brain cells, which when goes wrong is now believed to cause AD. A hypothesis has now been drawn that LRP sites in the synapses work with A2M to remove beta amyloid. If a mutation occurs in chromosome 12 and therefore A2M or if a deviation of APOe blocked the breakdown of Beta amyloid, plaques of Ab could form and would block the synapses which would slow down nerve signals and therefore present AD symptoms.

A new breakthrough in treating AD is to give patients acetylcholinesterase ( which breaks down acetylcholine) inhibitors to increase the levels of acetylcholine ( a neurotransmitter) in the synapse. Thus enhancing cholinergic activity in the regions of the brain that have been affected. Donepeizine is a drug used to inhibit acetylcholinesterase. A vaccine is being developed which prevents the build up of amyloid on the brain as plaques, however as yet tested on mice has proven that when the vaccine that is made up of amyloid � peptides is used to break down amyloid and destroy the plaques there has been no improvement of the brains function, however with ongoing research this could become a major lead into the prevention, treatment or even cure of AD.

Vitamin B12 acts as a ‘methyl’ donor during many reactions. The methyl group is added to a chemical known as homocysteine, this addition converts it to methionine. Methionine is needed to synthesise choline. A lack of choline leads to impaired fatty acid synthesis and decreased production of myelin which is the sheath that covers nerves. A reduced level of myelin sheath will result in the dysfunction of the nervous system, the plaques are also said to destroy the myelin. Vitamin B12 deficiency is more common in the elderly people which would also help to explain why AD is more common in older people.

Scientists in Japan have now stated that it is possible that a daily vitamin E supplement could stop the brain from generating diseases such as AD. Scientists believe that oxidative stress is now linked to brain diseases such as AD, it is thought that oxidative stress is caused by the toxic effect of highly reactive oxygen molecules known as free radicals which can damage cells and DNA. Evidence suggests that this may be responsible for progressive degenerative diseases such as Alzheimer’s. It has been discovered that vitamin E is an antioxidant that neutralises free radicals, this will prevent damage of cells etc. Vitamin E has been tested on mice with degenerative neurological diseases and has improved mental function, this offers us a very promising lead to helping AD.

A link has now been put forward that the hormone oestrogen may protect younger women that are at risk of inherited AD. The hormone oestrogen is a powerful nutritive factor for the nervous cells and are said to aid the ‘neuroplasticity’ which is the repairing of the capacity of our nervous system. This investigation is in its early stage and introducing oestrogen-only hormone supplements has been linked to cancers. At this stage of tests it is only slowing down the AD degradation and not reversing it. Ongoing tests in all of these links are being investigated and the future for AD could be very promising.


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