Alzheimer’s Disease:

Alzheimer's disease is one of the most common problems among the aged. It is devestating for the sufferer, but perhaps more so for the family and friends.

Symptoms:

Alzheimer’s disease has initially innocuous symptoms which appear no different to the normal effects of ageing. However, these symptoms progress to a chronic state. In the early stages, there is memory impairment for recent events and spatial disorientation (e.g., the inability to find objects). Impaired concentration occurs too. Patients can become more aggressive and depressed. Later symptoms are much more severe. All aspects of memory fail, and aphasia (loss of language), apraxia (impairment of purposeful movement), and agnosia (inability to recognise objects) develops. Dementia insofar as judgement and abstract thought also develops. There is just a general impairment of all intellectual function and patients become incapacitated and wasting ensues.

Neuropathological Observations:

Patients appear to have shrinkage of gyri and enlargement of ventricles in the brain. The shrinkage in the frontal and temporal lobes is in the range of 20-30% when the disease has really developed. There is a similar loss of white matter. Imaging techniques have shown in living patients degeneration of tissue in the cerebral cortex (in the frontal, parietal, and temporal lobes), and the amygdala and hippocampus. This cell loss correlates with the degree of dementia and is much greater than normal ageing. There are microscopic abnormalities in neuronal tissue as well, such as plaques and neuronal tangles. There is also up to a 70% loss in the chemical CAT from the temporal and parietal lobes, and the hippocampus. CAT is important to normal brain function. PET has shown that early in the disease, sufferers have hypermetabolism in affected cortical areas. This probably leads to cell death, and may be the result of a compensatory increase for the loss of other cells.

Causes:

There may be some genetic factor at work here since some families have high incidences of Alzheimer’s. However, genetics may not be a major cause because the disorder can occur sporadically. An environmental toxin may be at work, but nothing has really been identified. Studies have linked aluminium to the illness, since it accumulates in the cells of affected areas. But it cannot be said if the aluminium is causative, or a result of the illness. There may be a link to head injuries, as boxers can develop a similar dementia to Alzheimer’s. There is also a “nasal infection theory”. Since Alzheimer’s effects the areas with links to the olfactory system, such as the amygdala, hippocampus, and sensory association areas, whereas it leaves other areas (like the primary motor and visual cortices) untouched, it has been suggested that some toxin may enter through the olfactory bulb and cause this degeneration. However, the nature of such a toxin is unknown, and the olfactory system is only effected in the later stages of the illness. Nasal infection theory has been widely rejected. Given that there are several possible causes, it could, of course, be the case that there are several ways the same disorder could be produced.

Treatment:

There is no treatment for Alzheimer's. The degeneration cannot be halted. Methods to improve the memory problems have been made, but at the neglect of the anti-social behaviour sufferers have. Hydergine causes some improvement to cognitive function by altering neurotransmitters, blood flow, and oxygen usage. The outlook is a little bleak, but the best hope is trying to find the root of the degeneration so that preventative and corrective action can be taken.

Bibliography:

"Brain, Biochemestry and Brain Disorders", P. G. Strange, Oxford University Press, 1992