Common drug could prevent Alzheimer’s disease

A groundbreaking study has discovered that a widely-used medication could help prevent Alzheimer’s symptoms.

However experts suggest it may need to be administered almost two decades before the condition can even be detected through the earliest diagnostic tests.

For some time now, researchers have understood that Alzheimer’s disease is characterised by the build-up of harmful proteins within the brain.

Current medications available to Alzheimer’s patients work by removing some of these protein fragments, but levetiracetam, a commonly prescribed epilepsy drug, can actually halt the build-up before it begins.

The groundbreaking Northwestern University research identified precisely when and where these damaging fragments begin to gather, leading to the revelation that this seizure medication, which has been in clinical use for decades, can prevent this accumulation.

This breakthrough has paved the way for future research to gain deeper insights into the plaque formation that triggers Alzheimer’s and develop new therapeutic approaches for the condition.

One challenge identified by the research team is that levetiracetam is metabolised extremely rapidly by the body. Scientists are now developing an improved formulation of the medication that would remain active for longer periods and be more specifically targeted at preventing plaque formation.

« In our 30s, 40s and 50s, our brains are generally able to steer proteins away from harmful pathways, » said the study’s corresponding author Jeffrey Savas, PhD, associate professor at Northwestern University Feinberg School of Medicine.

« As we age, that protective ability gradually weakens. This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer’s, too many neurons go astray, and that’s when you get amyloid-beta 42 production. And then it’s tau (or ‘tangles’), and then it’s dead cells, then dementia, then neuroinflammation – and then it’s too late. »

One possible drawback the research identified is that levetiracetam would need to be administered remarkably early to prove effective. In certain instances, individuals at heightened risk of Alzheimer’s might need to begin treatment as much as 20 years before current diagnostic tools can even detect slightly raised protein concentrations in the brain.

The professor added: « You couldn’t take this when you already have dementia because the brain has already undergone a number of irreversible changes and a lot of cell death. »

Due to this constraint, those with rare genetic versions of Alzheimer’s would be the main group to benefit from these findings. This includes patients with Down syndrome, as over 95% of people with this condition will go on to develop Alzheimer’s.

The Northwestern research utilised genetically modified mouse models, cultured human neurons and human brain tissue from deceased patients with Down syndrome who passed away in their 20s or 30s from road accidents or other incidents.

Savas stated: « By obtaining Down syndrome patient brains from people who died in their 20s or 30s, we know they would have eventually developed Alzheimer’s, so it gives us an opportunity to study the very initial early changes in the human brain.

« That is what we and others call the paradoxical stage of Alzheimer’s disease, which is that before synapses are lost and dementia ensues, the first thing that happens is presynaptic proteins accumulate. Conceivably, if you started giving these patients levetiracetam in their teenage years, it could actually have a preventative therapeutic benefit. »