brain and dna strand
New research suggests that reducing the expression of the ApoE gene may stop the brain damage associated with Alzheimer’s disease.

A new study published in the journal Nature has uncovered a new role for a gene known to be key in the development of Alzheimer’s disease: ApoE. This newly gained understanding gives researchers a novel therapeutic target, which, they hope, will soon enable them to cure the condition.

The senior author of the new study is Dr. David Holtzman, head of the Department of Neurology at the Washington University School of Medicine in St. Louis, MO. The team – led by Dr. Holtzman – investigated the effect of the ApoE4 gene variant in the development of Alzheimer’s disease.

ApoE is a gene responsible for creating the protein apolipoprotein E, which – in combination with fats – forms lipoproteins. The latter carry cholesterol through the bloodstream.

ApoE has different variants, or alleles: e2, e3, and e4. Studies have shown that ApoE e4 (ApoE4) puts carriers at a dramatic risk of developing Alzheimer’s disease.

In fact, people with one copy of the gene are two to three times more likely to develop this kind of dementia, while those with both copies of the gene are 12 times more likely to have the disease.

Additionally, studies of brain pathology have shown that people with ApoE4 have more of the amyloid beta plaques accumulated in the brain. Beta-amyloid is a sticky protein that clumps together, blocking neuron-to-neuron signaling in Alzheimer’s patients.

So, while it is known that ApoE4 is somehow crucial in Alzheimer’s disease, the mechanism whereby this gene contributes to disease formation remains unclear.

The new research by Dr. Holtzman and his colleagues sheds some light on this mechanism. Their findings suggest that ApoE4 may “work” by exacerbating the damage done by a different protein associated with Alzheimer’s: tau.

ApoE amplifies tau damage in mice

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