Science/Tech

Genetic Basis Of Late-Onset Alzheimer's Discovered: Scientists Identify Potential Treatment

Alzheimer's Disease
Discovering the genetic basis of Alzheimer's, scientists are using this knowledge against the disease in new treatment efforts. Alzheimer's | Flicker

Alzheimer's disease affects one in eight elderly Americans. The disease is thought to simply be a part of getting older; as one ages, the brain loses some of its function, often leading to dementia and Alzheimer's. Late-onset Alzheimer's disease, however, is not as easily explained by aging.

A new study indicates that late-onset Alzheimer's disease has a genetic basis.

Scientists are still trying to find the pathway of events in nerve cells and brain tissues that lead to Alzheimer's. However, differences in the age of onset indicate that different changes occur. Early onset of Alzheimer's disease occurs before the age of 60, is known to run in families, and progresses quickly. Late onset, on the other hand, occurs after the age of 60, may not run in families, and progresses slowly. Both types of Alzheimer's disease cause changes to memory, language, and behavior, but less is known about late onset, as it progresses too slowly to be diagnosed earlier for study.

Late-onset Alzheimer's disease has now been linked to the presence of a gene that codes for a protein called APOE4. The protein is found to prevent the brain from fixing the molecular cause of dementia abundant in Alzheimer's patients. Most forms of Alzheimer's develop as a result of neurodegeneration, which occurs as a result of accumulations of proteins, which ought to be dispersed, in nerve cells. These accumulations are called amyloid-β (Aβ) plaques.

The plaques form in nerve cells and prevent them from communicating with each other. Nerve cell communication is crucial for cognitive health. As a result, this type of degeneration is a hallmark of Alzheimer's disease.

This study indicates that APOE4 proteins made as a result of the particular gene lead to late-onset Alzheimer's disease. This is because the APOE4 protein will prevent other regulatory proteins from dissolving the Aβ plaques and maintaining brain health. Accumulation of Aβ plaque leads to dementia and Alzheimer's, and neurological function becomes compromised.

Researchers found that those who carry the APOE4 gene can be over 10 times more likely to develop late-onset Alzheimer's disease. They also established that in the absence of the APOE4 gene, the likelihood of late-onset Alzheimer's disease significantly decreased, and the presence of the AB plaques indicative of Alzheimer's were absent.

Finding a genetic basis of an incurable disease like Alzheimer's is promising, as drugs can be targeted to specific genes.

Researchers tested a possible therapy, the drug levetiracetam. Because it prevents seizures, levetiracetam is a drug commonly used to manage epilepsy and some depressive mood disorders like bipolar disorder. Levetiracetam was found to inhibit the activity of APOE4. As a result, it prevents formation of AB plaques and the Aβ molecules that are precursors for the dangerous plaques. This is promising, as it essentially reverses the cause of Alzheimer's disease. The drug has proved worthy of further study.

 

Source: Rhinn H, Fujita R, Qiang L, Cheng R, Lee JH. Integrative genomics identifies APOE e4 effectors in Alzheimer's disease. Nature. 2013.

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