There are three commonly known types of Alzheimer’s disease. They include:
Early-onset Alzheimer's
This is a rare form of Alzheimer's disease in which people are diagnosed with the disease before age 65. Less than 10% 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 are often in their mid- to late 40s or early 50s when symptoms first appear.
Younger people who develop Alzheimer's disease have more of the brain abnormalities that are associated with it. Early-onset Alzheimer's appears to be linked with a genetic defect on chromosome 14, to which late-onset Alzheimer's is not linked.
Younger people who develop Alzheimer's disease have more of the brain abnormalities that are associated with it. Early-onset Alzheimer's appears to be linked with a genetic defect on chromosome 14, to which late-onset Alzheimer's is not linked.
Mutations of three genes, namely presenilin 1, presenilin 2, and amyloid precursor protein, are associated with Early Onset Alzheimer’s disease. These genes in isolation do not cause Alzheimer’s, however, mutations of these genes, can cause the disease.
Changes in the brains of younger people affected by Alzheimer’s disease are microscopic, involving twisting of nerve cells “known as neurofibrillary tangles” and formation of structures called plaques by a sticky protein called beta amyloid. These plaques and tangles tend to damage healthy brain cells leading to shrinking and atrophy.
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.
Individuals with early-onset Alzheimer's disease will exhibit many of the same symptoms as those whose disease appears later in life. Memory loss, confusion, personality changes and difficulties performing simple tasks are all very common symptoms and as the disease progresses emotional and social withdrawal is the norm. Anyone who has this combination of symptoms should see a physician as soon as possible.
Alzheimer's diagnosis usually comes as a result of ruling out all other possibilities. The only way to biologically diagnose it is to examine brain tissue under a microscope, which is typically done only after death.
Late-onset Alzheimer's
This is the most common type of the disease affecting about 90% of all those with Alzheimer’s. It affects people over the age of 65 with around 50% of all people over the age of 85 suffering from it. And the likelihood of developing late-onset Alzheimer’s doubles every five years after the age of 65. Late-onset Alzheimer's disease may not be hereditary.
It is also known as “sporadic Alzheimer’s” because it can affect any elderly person with no other common link other than the fact that they are all over 65.
Late onset Alzheimer’s causes memory loss, confusion and difficulties in carrying out even the simplest tasks. Eventually a person will need constant care as they will be unable to look after themselves.
On average people live roughly eight to ten years after diagnosis. Sometimes with sporadic Alzheimer’s, because it affects people so late in life, another disease associated with old age could also be the cause of death.
There is no cure and the jury is still out as to why some people get it and others don’t. It is indiscriminate of race, color, creed and lifestyle. In fact the only thing sufferers have in common appears to be old age.
Unfortunately finding genes for incredibly complex conditions like sporadic Alzheimer’s is a complicated business as there appears to be no link between who gets it and who doesn’t. So far researchers haven’t come across one single common factor to determine the eventual development of late-onset Alzheimer’s. What they have done, however, is identify a gene which may be a risk factor. Apolipoprotein E (ApoE) is interesting in that it has both a negative and positive side in the development of Alzheimer’s. The e4 type of the gene is found to carry a higher risk of Alzheimer’s while the e2 type is believed to offer protection against it. Having this gene doesn’t necessarily mean that a person will get Alzheimer’s – what it does mean is that it may increase their risk. Environmental factors, lifestyle and toxins can all play a part in weakening genes and making a person more susceptible to an illness.
Sporadic Alzheimer’s is a very difficult and complex disease for researchers because there is no real rhyme or reason to it. Until they can come up with an identifying factor other than age, there will be no cure.
Familial Alzheimer's disease (FAD)
This is a form of Alzheimer's disease that is known to be entirely inherited. In affected families, members of at least two generations have had Alzheimer's disease. FAD is extremely rare, accounting for less than 1% of all cases of Alzheimer's disease. It has a much earlier onset (often in the 40s) and can be clearly seen to run in families. In some extremely rare cases people in their 30s have been known to develop it.
Histologically, familial AD is practically indistinguishable from other forms of the disease. Deposits of amyloid can be seen in sections brain tissue (visible as an apple-green yellow birefringence under polarized light). This amyloid protein forms plaques and neurofibrillary tangles that progress through the memory centers of the brain. Very rarely the plaque may be unique, or uncharacteristic of AD; this can happen when there is a mutation in one of the genes that creates a functional, but malformed, protein instead of the ineffective gene products that usually result from mutations.
This type is genetically inherited due to a fault on chromosomes 1, 14 or 21. When this happens roughly 50% of the offspring of these sufferers will carry the genetic fault and all of them will go on to develop Alzheimer’s.
Mutations in three different genes -- the amyloid precursor protein (APP) gene and the presenilin 1 and 2 (PSEN1 and PSEN2) genes -- have been discovered in families with early-onset familial Alzheimer's disease. Taken together, these mutations only account for about 20-50% of familial Alzheimer's, indicating that other genes remain to be found in this disorder.
The APP gene encodes the beta-amyloid protein which accumulates abnormally in the brain in Alzheimer's disease. The protein products of the PSEN1 and PSEN2 genes interact with proteins are involved in signaling processes within and between cells.
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