Dementia is the loss of intellectual capacity to the extent that normal social and occupational functions can no longer be carried out.
Alzheimer's disease is a progressive form of dementia characterized by the grandual deterioration of intellectual abilities such as memory, judgement, capacity for abstract thought, and other higher-level cognitive functions.
The onset of presenile Alzheimer's disease is usually after the age of 40 and consists of three main phases. The first phase lasts for 2 to 3 years, and is characterized by failing memory, muddled inefficiency over mundane tasks as well as spatial disorientation. Mood disorders are prominent and take the form of perplexity, agitation and restless hyperactivity. In the second phase, there is greater intellectual and personality deterioration. Focal symptoms also appear. In the third (or terminal) stage, there is extreme apathetic dementia in which the patient becomes bedridden. Neurological disabilities may develop, such as spastic hemiparesis (hemispheric paralysis) or severe striatal rigidity (irregular streaks or patches of nerve cell loss in the cerebral cortex) and tremor.
Histologically, there is degeneratoin and loss of nerve cells which affects the outer three cortical layers and the thalamus as well as secondary glial proliferatoin (the rapid growth of the plial cells which perform support tasks such as production of the myelin sheath and nutritional support). Senile plaques and neurofibrallary tangles are characteristic of Alzheimer's disease and the neurofibrillary tangles occur in grey matter, particularly in the hippocampus and amygdala. The senile plaque lie within the nerve cells and often fill the entire cell body, and may have no core and appear to consist on ly of granular or filamentous fragments. Cortical atrophy (the wasting away of the cortex) is also present and tends to affect the frontal and temporal lobes. The white matter shows axonal degeneration, hyperplasia (the increase in organ size caused by an abnormal increase in number of cells) of astrocytes as well as fibrous gliosis (the replacement of neuron cells by glia cells). Other characteristic features include shrinking of the brain, flattening of the gyri, widening of the sulci and enlarging of the ventricles.
The walls of intracerebral arteries tend to thicken with advancing age. The collagen in the outer layers become more prominent which causes the wall and surrounding tissue to die and, in most cases, disintegrate. There is an interference of cerebral cirulation which is caused by blockage of the common carotid, inner carotid and venebral arteries in the neck and bony channels of the skull. With regards neuro-chemistry, there are also deficiencies in neurotransmitters such as acetylcholine, noradrenaline, serotonin and somatostatin.
there seem to be certain general triggers for Alzheirmer's diseas such as minimal brain damage from head injury, infection and surgery. However, the illness is usually already in existence, and these "triggers" or precipitants have merely revealed the problem.
As so far as treatment is concerned, there is no cure. However, cutting edge research in stem cell development is showing promising results for counteracting the degenerative effects of Alzheimer's Disease.