Types of Alzheimer’s Disease
Alzheimer’s disease is the most common cause of dementia among older people. It is marked by progressive and, at present, irreversible declines in certain cognitive functions. These impairments may include declines in memory, time and space orientation, abstract thinking, the ability to learn and carry out mathematical calculations, language and communication skills, and the performance of routine tasks.
There are several Types Of Alzheimer’s Disease
Early-onset Alzheimer’s
This is a rare form of Alzheimer’s disease in which individuals are diagnosed with the disease before age 65. Less than 10 percent of all Alzheimer’s disease patients have this type. Because they experience premature aging, people with Down syndrome are particularly at risk for a form of early-onset Alzheimer’s disease. Adults with Down syndrome often are in their mid to late 40s or early 50s when symptoms first appear.
A condition called myoclonus which causes muscle twitching and spasms is much more common in people with early onset than those who develop the disease later in life. These will all combine to make it very difficult for someone in the younger age group to continue to work or even take part in normal family life.
Younger people who develop Alzheimer’s disease have more of the brain abnormalities that are associated with Alzheimer’s disease. Early-onset Alzheimer’s appears to be linked with a genetic defect on chromosome 14, to which late-onset Alzheimer’s is not linked. A condition called myoclonus – a form of muscle twitching and spasm – is also more commonly seen in early-onset Alzheimer’s than in late-onset Alzheimer’s.
Late-onset Dementia
Argyrophilic grain disease (AgD) is a late-onset dementia morphologically characterized by the presence of abundant spindle-shaped argyrophilic grains (ArG) in neuronal processes and coiled bodies in oligodendrocytes. AgD changes consist of the microtubule-associated protein tau in an abnormally and hyperphosphorylated state and are mainly found in limbic regions, for example, in the hippocampus, the entorhinal and transentorhinal cortices and the amygdala.
Several studies have suggested that environmental factors during childhood may contribute to the likelihood of developing dementia. But the relationship between childhood intelligence and dementia in later life hasn’t been fully explored because few childhood intelligence test records are available for people who are old enough to have experienced the risk period for dementia.
Familial Alzheimer’s
A proportion of cases of Alzheimer disease show familial aggregation with a pattern of vertical transmission compatible with autosomal dominant inheritance. Isolation of the genetic defect causing this form of Alzheimer disease, which may elucidate the biochemical mechanisms underlying the pathogenesis of the Alzheimer disease phenotype, can theoretically be achieved by first defining the chromosomal location of the disease gene(s) by classical genetic linkage studies in large families segregating this disorder.
In a family with autopsy-confirmed Alzheimer disease, the authors found a mutation in the presenilin 2 (PS2) gene (PSEN2) that predicts a methionine-to-isoleucine change at PS2 residue 239 (M239I), at which a change to valine was known in another family. Phenotypic expression of M239I was highly variable, with disease onset between age 44 and 58 years, and two nonaffected mutation carriers at age 58 and 68 years.
