Healing Connections

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An international group of scientists found that a new gene called calcium homeostasis modulator 1 (CALHM1), with a previously unknown function, is linked to late-onset Alzheimer’s Disease making this the second discovery of a strong genetic risk factor for the disease.

The study was the work of researchers from the US, France, Italy, UK, and Australia, led by Dr Philippe Marambaud of The Feinstein Institute for Medical Research, Manhasset, New York, and Albert Einstein College of Medicine, Bronx, New York, and is published online in the June 27 issue of the journal Cell.

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by the build up of senile plaques made of amyloid-beta peptides and a massive loss of neurons or brain cells.

The early-onset form of Alzheimer’s is thought to be linked to a few dominant gene mutations, but the vast majority of late-onset cases are believed to stem from complex interactions of genes and environment factors.

The study reports that CALHM1 is active mostly in a calcium channel in part of the brain that is affected early in the development of Alzheimer’s. The researchers discovered that variants of CALHM1 influence levels of calcium, amyloid-beta peptides, and susceptibility to the disease.

This study coincides with the publication of another paper in the 26th June issue of a sister journal Neuron, where scientists report finding an imbalance of calcium in early-onset Alzheimer’s Disease that is linked to a calcium release ion channel.

Marambaud said in a statement that:

“We are very excited about the idea that CALHM1 could be an important target for anti-amyloid therapy in Alzheimer’s disease.”

He said because CALHM1 is restricted to the brain, drugs that target it would most likely have fewer side effects, which is a big question mark with drugs that are currently being trialled because these target enzymes involved in production of amyloid-beta peptides, and these enzymes are also present in other parts of the body.

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