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New Research on Genetic Link to Alzheimer’s Offers Hope

June 27
09:23 2018

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Alzheimer’s is something everyone fears as they grow older. About 1% of all Alzheimer’s cases are directly caused by a gene mutation. This mutation causes early-onset Alzheimer’s which is also known as familial Alzheimer’s disease (FAD).

There is another genetic link to the development of Alzheimer’s. While this mutation doesn’t directly cause Alzheimer’s like that of FAD, it does increase the likelihood that a person will develop the deadly disease.

The mutation occurs with the APOE gene, and according to one source:

“There are three types of the APOE gene, called alleles: APOE2, E3 and E4. Everyone has two copies of the gene and the combination determines your APOE “genotype”—E2/E2, E2/E3, E2/E4, E3/E3, E3/E4, or E4/E4. The E2 allele is the rarest form of APOE and carrying even one copy appears to reduce the risk of developing Alzheimer’s by up to 40%. APOE3 is the most common allele and doesn’t seem to influence risk. The APOE4 allele, present in approximately 10-15% of people, increases the risk for Alzheimer’s and lowers the age of onset. Having one copy of E4 (E3/E4) can increase your risk by 2 to 3 times while two copies (E4/E4) can increase the risk by 12 times.”

“Despite this association, the National Institutes of Health only recommends genetic testing for APOE status to advance drug research in clinical trials. APOE4 is just one of many risk factors for dementia and its influence can vary across age, gender, race, and nationality. For example, having one copy of the E4 allele may pose more risk to women while having two copies seems to affect men and women similarly.”

However, if you have been told that you have the APOE4 gene mutation, there may be hope on the horizon.

Researchers from the University of California, San Francisco and Gladstone Institute of Neurological Disease studied the APOE4 mutation and why it can increase the chances of developing Alzheimer’s:

‘Their observations showed that APOE ε4 triggers the development of various Alzheimer’s pathologies in brain neurons, including an increase in APOE fragmentation, tau phosphorylation, production of beta-amyloid (a protein that accumulates into harmful plaques), and the degeneration or loss of GABAergic neurons (which affect neurotransmitters).”

In studying how the APOE4 mutation works, they discovered a way to neutralize it:

“First, they used gene editing to convert the harmful form of the APOE gene to the neutral form, which removed the resulting protein’s detrimental effects. In addition, the researchers used a small-molecule ‘corrector’ they had previously developed to turn the ApoE4 protein into an ApoE3-like protein. The results were similar: Alzheimer’s pathologies were reduced, and the cells’ normal function was restored.”

“The authors noted that the ApoE4 protein results in beta-amyloid production in human but not mouse neurons, and that conversion of ApoE4 to ApoE3 by gene editing significantly lowered beta-amyloid production, consistent with a specific effect of ApoE4.”

This is still the early stage of research, but it offers another source of hope for those with the mutation who are worried about their increased risk of developing Alzheimer’s. It will take a few years to further test and then get FDA approval for use, but there is light on the horizon, along with a number of other advances that have been made in Alzheimer’s research.

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HLA Staff

HLA Staff

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