In a new study from the RIKEN Center for Brain Science, researchers have discovered that the protein α-endosulfine (ENSA) is involved in the development of Alzheimer’s disease.
They showed that eliminating this protein entirely or using drugs to block its function reduced physical changes in the brain associated with the disease and improved memory.
Drug therapy that aims to block ENSA activity could be a more effective treatment than what is currently available, as well as being cheaper.
The hallmark of Alzheimer’s disease in the brain is the accumulation of amyloid β peptide (Aβ). For years, researchers have been trying to determine how and why this happens.
In the study, the team found both Aβ accumulation and memory deficits similar to what is seen in humans.
They found reduced levels of the enzyme neprilysin, which itself is caused by reduced levels of the hormone somatostatin.
Levels of both neprilysin and somatostatin go down as we age, which can explain why Alzheimer’s disease usually strikes older people.
In the study, the team focused on treating Alzheimer’s disease by figuring out how somatostatin controls neprilysin levels in the brain.
They found that somatostatin normally keeps ENSA in check, which in turn keeps neprilsyin levels high, allowing Aβ to be destroyed before it accumulates.
They then showed that abnormally high levels of ENSA could be an as yet unidentified symptom or biomarker of Alzheimer’s disease.
The researchers reasoned that helping the channel stay open would combat the excess ENSA that we observed in Alzheimer’s disease.
To test this theory, they fed the model mice with diazoxide—a drug that activates the KATP channel—and tested their memory.
They found that while the untreated Alzheimer’s disease model mice exhibited their characteristically poor memory, the treated model mice performed just as well as normal mice.
A look at the brains of the treated mice showed that they lacked the hallmark Aβ plaques.
These findings point directly to a potential way of preventing and treating Alzheimer’s disease.
On top of that, compared with Aβ-targeting immunotherapy, such as the drug aducanumab, which was recently approved by the FDA, synthetic agonists for the KATP channel are less expensive and would be more acceptable to aging societies around the world.
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The study is published in Molecular Psychiatry.
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