Alzheimer’s disease and broader dementia are a growing epidemic challenging care for global ageing populations. Characterised as a neurodegenerative disease, Alzheimers involves the degeneration of the brain and a subsequent loss of cognitive function. Memory loss, confusion, and delusion all plague patients with Alzeihmers, and so too, the family and caregivers who care for these individuals. As this disease becomes more prevalent amongst our future ageing population, intriguing research is coming forward on the causes of Alzheimer’s and even some of the ways to prevent it. A review by Ansab Akhtar and Sangeeta Pilkhwal Saw out of Punjab University in Chandigarh, India is presenting some useful insight on the effects of insulin to the brain.
In order to understand this, however, we must first assess the two largest factors that contribute to the neurodegeneration in Alzheimer’s disease. The first is amyloid-ꞵ plaques. ꞵ-amyloid is a small protein that can misfold and connect with other ꞵ-amyloids to form a plaque-like formation outside of a cell. When this plaque forms, it inhibits the binding of insulin to its receptors in the brain. The second contributor to Alzeimhers important in understanding the effects of insulin are neurofibrillary tangles or NFTs. NFTs arise when Tau proteins become hyperphosphorylated leading to tangle formation in microtubule networks which leads to their collapse. In other words, look at Tau protein as a Jenga block at the very bottom of a tower that resembles the framework of a cell, otherwise known as microtubules. When this block is removed, the microtubule tower falls and so does the cell that it provided a framework for. NFTs are much like the fall of a Jenga tower.
Insulin is crucial to the action of both amyloid-ꞵ and NFTs. Insulin is responsible for regulating blood sugar throughout the body but it plays a valuable role in protecting the neurons in the brain. The review by Akhtar and Saw provides insight into how the brain developing resistance to insulin is related to the formation of amyloid-ꞵ plaques and NFTs. The first figure placed in the review shows the various ways the insulin signalling pathway can be affected. Many of the molecules inside the cell can contribute to NFT formation internally whilst also allowing amyloid-ꞵ to be produced which can stop insulin signalling all together at its receptor. When there is dysfunction of this insulin pathway, the neurons do not function optimally and often undergo apoptosis, which is programmed cell death.
Understanding insulin resistance is valuable in understanding Alzheimers and treating it in our future. Processed food products are used by societies across the globe to ensure cheap and abundant food. This abundance, however, has led to metabolic syndrome and an increase in insulin resistant diabetes in our communities. Being one of the largest contributors to these problems, changing our diets should be a starting point. Whole, unprocessed foods take more metabolic effort to digest and minimise the blood sugar spikes we see from processed counterparts. Much like how they slow down digestion, these whole foods also slow down our day to day lives. Taking more time to focus on our diet also allows us to make greater effort towards our physical activity. A healthier society may see less insulin resistance which may be one of the first steps we can make to stopping Alzheimer’s disease in its tracks.
Ansab Akhtar and Sangeeta Pilkhwal Saw, “Insulin signaling pathway and related molecules: Role in neurodegeneration T and Alzheimer’s disease” Neurochemistry International 135, (2020)
