Evaluating Senescence-Targeted Approaches In Alzheimer’S Disease: What We Know And What Lies Ahead
As we age, some of our cells can enter a state called “senescence.” These cells stop dividing but don’t die off; instead, they linger and release a cocktail of inflammatory and toxic substances. This cellular “zombie” state contributes to the aging process and plays a significant role in age-related diseases, including Alzheimer’s disease.
Recent research highlights that these senescent cells accumulate in the brains of individuals with Alzheimer’s, contributing to the chronic inflammation and damage seen in the disease. Studies in animal models have shown that removing these problematic cells can lead to a reduction in key Alzheimer’s pathologies, such as amyloid plaques and neurofibrillary tangles, and even improve cognitive function.
This understanding has opened up exciting new avenues for treatment. Scientists are exploring two main strategies: “senolytics” and “senomorphics.” Senolytics are compounds designed to selectively eliminate senescent cells, much like a targeted clean-up crew. Examples include drugs like dasatinib, quercetin, fisetin, and navitoclax.
Senomorphics, on the other hand, aim to suppress the harmful substances released by senescent cells without necessarily killing them.
While early human studies suggest these senescence-targeted interventions are feasible, there are still significant hurdles to overcome. Key challenges include ensuring these drugs can effectively reach the brain, determining the best dosages and treatment schedules, confirming their long-term safety, and developing reliable ways to identify which patients would benefit most and how to monitor treatment success.
Despite these challenges, these innovative approaches hold great promise as complementary treatments to existing therapies for Alzheimer’s, offering a multi-pronged attack against this complex disease.
Source: link to paper