Breakthrough Reveals New Treatment Target For Alzheimer’s

Despite being the most prevalent neurodegenerative disease globally, Alzheimer’s disease has been notoriously challenging to prevent, let alone cure. The biggest hurdle for delivering drugs into the brain is the blood-brain barrier. These tiny blood vessels form tight junctions between brain cells to regulate the movement of molecules from the blood into the brain.

A growing body of evidence now shows that insulin resistance may also be implicated in Alzheimer’s disease. In post-mortem exams of human and animal brains with Alzheimer’s disease, changes in the brain’s insulin-binding receptors seem to correlate with learning and memory deficits. Other reports suggest that impaired insulin signaling may be associated with the accumulation of beta-amyloid and tau neurofibrillary tangles, which are characteristic of Alzheimer’s disease.

If insulin-binding receptors are impaired in Alzheimer’s, it is possible that drugs that target those receptors may be able to slow, or prevent, cognitive decline. The first question researchers had to answer, however, was where in the brain are these receptors located. To answer this question, Leclrec et. al began their study by examining brain tissue samples from healthy individuals without dementia. They were surprised to find that there were no insulin-binding receptors in the brain itself.

When they examined brain samples from individuals with Alzheimer’s disease, however, the number of insulin-binding receptors found in the blood-brain barrier was considerably reduced. Leclerc et. al also observed this trend in mice models with genetic mutations associated with Alzheimer’s disease. Not only were there fewer insulin-binding receptors but the activation of these receptors was also blunted.

This presents a promising treatment approach for Alzheimer’s disease. Without having to cross the blood-brain barrier, drugs that target insulin-binding receptors within the blood vessels directly may be able to influence brain activity. However, it is still not well understood how insulin resistance contributes to cognitive decline, nor how stimulating these receptors would improve symptoms.

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