2. Sporadic Alzheimer's - Late Onset Alzheimer's

Sporadic Alzheimer's, also known as Late Onset Alzheimer's, is the most common form of Alzheimer's by far, and tends to occur much later in life than FAD. It can affect adults of any age, but it usually occurs after age 65.

This form of Alzheimer's can affect people who may or may not have a family history of the disease.

There is currently no evidence that autosomal dominant inheritance of mutated genes causes Sporadic or Late Onset Alzheimer's. However, genetics does appear to play a significant role in the development of this far more common form of the disease.

Different variations, or alleles, of particular genes produce variations in inherited characteristics, such as height, skin color, eye color, blood type, and so on.

In the early 1990s, researchers at Duke University in Durham, North Carolina, found an increased risk for late-onset Alzheimer's in people who inherited one or two copies of a particular variation of a gene called apolipoprotein E (APOE) - the variation known as APOE e4.

Apolipoprotein E is a protein that has various functions, such as helping the blood to carry cholesterol throughout the body.

This protein was found in neurons and other supportive brain cells (called glia) of healthy brains, but it is also found in excessive amounts with the plaques found in the brains of people with Alzheimer's.

Genetic Research

The National Institutes of Health (NIH) funded the pioneering research that led to the discovery of genes associated with Alzheimer’s disease. Researchers and scientists are unraveling the clues to the biological sequence of events in the development of Alzheimer's, by monitoring a range of proteins made by various genes.

Scientists observed the formation of amyloid plaques in mice, and the development and onset of Alzheimer's symptoms as the mice aged, by inserting mutated human APP genes into mouse eggs and raising the mice to adulthood. Scientists have developed many transgenicanimal models of Alzheimer's disease to understand how a complex array of pathways, both inside and between various cells, interact to affect the production of Alzheimer's plaques.

These transgenicanimal models provide a way to test a variety of different treatments to reduce the build-up of these plaques and slowing or halting the development of Alzheimer's.

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