Cell Dysfunction Linked To Development Of Alzheimer’s Disease

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Cell dysfunction is among one of the most glaring evidences linked to the degenerative Alzheimer’s disease that plagues millions of Americans and for which no known cure has been found.

Cell dysfunction identifies markers early on

This, after a study that highlighted the findings in the journal Neuron, revealed that people with a duplicate variant of the TREM2 genes were more likely to develop Alzheimer’s disease later on.

The study conducted by researchers from biotech company Genentech details their findings where suggest how a type of immune cell helps get rid of amyloid-beta aggregates that clump together to form plaque that result to Alzheimer’s disease in the brain.

It was in this study where they discovered the TREM2 mutations are able run counter to the clearing effects of these immune cells and may cause Alzheimer’s to worsen.

Two other proteins were identified that could also hinder immune cells like the TREM2 which are APOE and APOJ.

Mutated genes affect immune cells from fighting Alzheimer’s

“I think we’re only scratching the surface of what TREM2 does,” says Morgan Sheng, senior author and Vice-President of Neuroscience at Genentech.

Immune cells called microglia protect the brain and tests showed that these cells work efficiently to fight off plaque-building proteins from developing into Alzheimer’s. But in the presence of these mutated genes, it derails the clearing properties of the gene from slowing down or preventing genes from progressing into Alzheimer’s disease.

“Lipoproteins float around in the blood, and their purpose is to carry cholesterol or lipids from one cell to another—as we all know, too much LDL is associated with high cholesterol and increased risk of cardiovascular disease,” says Sheng. “Lipoproteins also exist in the brain, but less is understood about their role there.”

The researchers also found that macrophages found in people that carry the TREM2 variant associated with Alzheimer’s developed a decreased capability to engulf lipoprotein-amyloid beta complexes. It also showed that it would only take one copy of the TREM2 gene and not two to disrupt this clearing ability.

“Overall, these studies further point towards microglia as playing an important role in the pathogenesis of Alzheimer’s disease,” adds Sheng.

According to the Alzheimer’s Association, Alzheimer’s disease is the 6^th leading cause of deaths in the United States alone. Has already cost an estimated $236 billion maintenance and treatment medicines alone.

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