{"id":1170,"date":"2017-09-28T11:16:33","date_gmt":"2017-09-28T10:16:33","guid":{"rendered":"http:\/\/blogs.reading.ac.uk\/the-forum\/?p=1170"},"modified":"2021-11-15T11:06:45","modified_gmt":"2021-11-15T11:06:45","slug":"watchers-on-the-wall-microglia-and-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/research.reading.ac.uk\/research-blog\/2017\/09\/28\/watchers-on-the-wall-microglia-and-alzheimers-disease\/","title":{"rendered":"Watchers on the wall: Microglia and Alzheimer\u2019s Disease"},"content":{"rendered":"

By Laura Thei, University of Reading, UK<\/strong><\/p>\n

Reproduced with permission from The Physiological Society’s blog.<\/a><\/em><\/p>\n

The watch, worn by years of use, sits ticking on our table for the first time in two years. It has a simple ivory face and is the last memorabilia my partner has from Grandad Percy. Percy passed from us after a long personal battle with dementia, specifically Alzheimer\u2019s disease. It is in his name that my partner and I will take to the beautiful winding pathways beside the Thames, to raise money for the Alzheimer\u2019s Society.<\/p>\n

We will be taking part in a 7 km Memory Walk, with thousands of others, some my colleagues from the University, each sponsored generously by friends and families, each who has had their life touched by this disease in some way. Last year nearly 80,000 people took part in 31 walks, raising a record \u00a36.6 million. As a researcher in Alzheimer\u2019s disease, I am acutely aware of\u00a0every penny\u2019s impact<\/a>\u00a0in helping to solve the riddle of dementia.\u00a0<\/p>\n

Alzheimer\u2019s disease is ridiculously complicated. Oh, the premise is simple enough: two proteins, amyloid beta and phosphorylated tau, become overproduced in the brain and start to clog up the cells like hair down a plug. This causes these cells to be deprived of nutrients, oxygen and other vital factors that keep them alive. This eventually causes regional loss in areas specific to memory and personality. It\u2019s simple in theory, but the reality is that we still have much to learn.<\/p>\n

Current, extensive research is starting to answer these questions and whilst there is a growing list of risk factors \u2013 genetic (APOE4, clusterin, presenilin 1 and 2) and environmental (age, exercise, blood pressure) \u2013 confirmation only occurs when a brain scan shows the loss of brain region volume in addition to the presence of amyloid beta and tau. This means that by the time someone knows they have the disease, it\u2019s possible that it\u2019s already been chugging away at their brains for some time.<\/p>\n

So we need to push diagnoses earlier. To do that we need to look at the very early stages of the disease, down to a cellular level, to find out how we can prevent the build-up of amyloid and tau in the first place. This is what I, the group I\u2019m in, and many other researchers nationally and globally are striving to do.<\/p>\n

I am specifically focusing on the immune cells of the brain, microglia, and their contribution. Microglia are the most numerous cells in the brain. They act as the first line of defence, so their involvement and activation is often seen as an early sign of disease progression. Like all good defences, they tend to be alerted to damage before it becomes deadly. But, like the neurons (the basic building blocks of the brain), microglia are also susceptible to the disease. If they die, does that leave the brain more vulnerable to further insult? That is what I would like to know too!<\/p>\n

In a non-active state, microglia lie quietly surveying their local area of the brain. When activated by a threat to the brain, they cluster around the targeted area, changing shape in the process. They then enter one of two states. The pro-inflammatory state releases molecules that attack the harmful pathogens directly, and the anti-inflammatory state releases ones that promote healing and protection of the area.<\/p>\n

With Alzheimer\u2019s, microglia are activated by the accumulation of amyloid, not damage. They absorb the amyloid beta, and in the process, trigger the pro-inflammatory response. This then increases the permeability of the brain\u2019s blood supply, allowing immune cells into the brain to assist removal of the excess protein. However, in the brain of Alzheimer\u2019s patients, the amyloid beta production outdoes the microglia\u2019s ability to remove it. This creates a perpetual cycle of pro-inflammatory response, releasing molecules that can kill cells in the brain. It is unclear whether there is a threshold between beneficial or detrimental in the microglial response.<\/p>\n

Given the importance of microglia in neurodegenerative diseases, a new field of microglial therapeutics has recently emerged, ranging from pharmacologically manipulating existing microglia by switching their response status, to inhibiting microglial activation altogether. Continued research and clinical efforts in the future will help us to improve our understanding of microglial physiology and their roles in neurological diseases.<\/p>\n

We\u2019re making progress, but there\u2019s still a long way to go, which is why every penny counts!<\/p>\n","protected":false},"excerpt":{"rendered":"

By Laura Thei, University of Reading, UK Reproduced with permission from The Physiological Society’s blog. 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