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A novel therapy for Alzheimer’s?

The University of Copenhagen in Denmark has recently released a study examining a novel approach to treating Alzheimer’s disease. With a potential future crisis of the disease on India’s hands, any new knowledge on how to prevent the condition could be a vital lifeline.

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India’s looming dementia crisis


Two decades ago Alzheimer’s disease was considered relatively rare in India. However, current estimates place the number of patients with Alzheimer’s disease in India at around four million. India is entirely unprepared for a future in which the prevalence of Alzheimer’s disease rises sharply, according to the Alzheimer’s and Related Disorders Society of India (ARDSI). The ARDSI cites the lack of government policy in place to address the condition.

The four million figure could potentially triple by 2050. This would leave a wide section of the population potentially needing round-the-clock care. Besides the healthcare implication, this could also have economic consequences.

“Alzheimer’s carries with it significant economic and social costs. We need to intensify clinical research efforts to look for a cure for Alzheimer’s,” said Chirag Trivedi, President of Indian Society for Clinical Research.

Indians are living longer, which is good news. Unfortunately, they are also adopting unhealthier westernised diets and sedentary lifestyles. As a result, their risk of Alzheimer’s disease increases due to an abundance of unhealthy food and lack of physical activity. Promoting more traditional Indian diets rich in vegetables and antioxidant-containing spices could prove hugely beneficial to the population in the future. Healthy diets alone will not stop the rising numbers of dementia cases, and India, like the rest of the world, must be open to all research avenues to attempt to find a treatment for what is otherwise an incurable condition.


Mitophagy — the cleansing of the brain


The means by which Alzheimer’s disease occurs is still debatable. Genetic testing models implicate amyloid beta plaques, formed by aggregated amyloid beta proteins which proceed to cause dysfunction and cell death within brain tissue, such findings have been confirmed by the increased rate of Alzheimer’s disease in those with Down’s syndrome. The triplication of chromosome 21 in Down’s syndrome allows for another copy of the amyloid precursor protein (APP) gene, increasing amyloid burden and therefore Alzheimer’s risk.

Other suggested theories involve tangles within tau proteins, prions, inflammation, or even the fact that mental deterioration is simply a biological inevitability. Different individuals experience the process at different rates — some dying before it ever even begins to occur.

The Copenhagen study takes a novel approach, addressing the concept of mitophagy — the selective degradation of a cell’s mitochondria through autophagy. The study found that in brain cells of patients with Alzheimer’s as well as cells from Alzheimer’s induced mice and roundworms there was an accumulation of dysfunctional mitochondria.

It was also found that, by applying techniques to improve the ability of model organisms to begin efficient mitophagy again, the symptoms of Alzheimer’s disease were reduced.  “When the cleaning system does not work properly, there will be an accumulation of defective mitochondria in the brain cells. And this may be really dangerous,” said Vilhelm Bohr from the National Institutes of Health in the US. “The cleaning system is markedly weakened in cells from both humans and animals with Alzheimer’s…when we improve the cleaning in live animals, their Alzheimer’s symptoms almost disappear.”

While a direct association with Alzheimer’s disease has not yet been proven in any concrete manner, it is widely known that dysfunctions in mitophagy result in the death of nerve cells. For this reason it may be the case that the dysfunctional mitophagy is not the cause of Alzheimer’s disease, rather a potential result of it, eventually leading to the characteristic nerve cell death.

Further intertwining the studies findings with the already proposed mechanisms of Alzheimer’s was the finding that when normal mitophagy was restored, the aggregation and accumulation of the amyloid beta and tau tangles was slowed.

This could potentially point towards encouraging mitophagy as a potential new pharmaceutical target in slowing down the process of Alzheimer’s deterioration. As of yet , there are still no means to reverse the damage done — a process made far more difficult due to the complexity of the interactions between brain cells.

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