Alzheimer’s disease is a complex disorder, and its treatment and prevention methods are on the list of research. It’s a condition in which scientists have to solve many-piece puzzles to tackle this disorder.
How to handle and treat the dysfunction of brain cells is unsure to scientists. Numerous researches on Alzheimer’s disease are carried out by scientists.
Inflammation Of Alzheimer’s Disease On Brain And Immune System
A study was conducted on mice as a model to examine the epileptic activity in the brain that results in abnormal functioning caused by Alzheimer’s disease.
Their study shows there is multiple risk factor associated with Alzheimer’s disease-causing brain network and immune system dysfunction.
It is a disease that can trouble people after a certain age. However, the effects and age vary from person to person. New research in this direction is carried out by experts that have proven that inflammation on the brain can lead to severe issues triggering the worst impacts of this disease on an individual over a short period also.
Mainly, TREM2 is a genetic risk factor and stimulating key aspects of Alzheimer’s disease. According to the findings of Lennart Mucke, MD director of the Gladstone Institute of neurological disorders, suggest strategies treat and reverse Alzheimer’s disease abnormality related to brain network and immune system.
The research done by scientists could help patients by eliminating symptoms and reducing the ailment. An intriguing link between epileptic activity and nerve inflammation is known for chronic dysfunction in the brain. The underlying cause of the inflammation seems to be an accumulated amyloid protein referred to as plaque. Plaque is known to be a neuropathic mark of illness.
From the new study of Alzheimer’s related mouse model, researchers identified another critical driver of chronic brain inflammation that predicts a faster cognitive decline rate. Epileptic activity accelerates cognitive decline, but now this might be suppressed with the use of two therapeutic inventions, says Melanie Das, the Ph.D. lead scientist.
With the help of genetic engineering in a mouse model, the experts were able to prevent abnormalities by eliminating a protein tau causing neuron hyperexibilty at the same time. By treating the mice with the anti-epileptic drug levetiracetam, alteration of nerve networking and immune cells can be reversed.
Recent clinical trials in Mucke’s lab resulted in cognitive benefits in patients with protein tau lowering therapeutic. This study assures a promising statement for patients at the early stages of Alzheimer’s disease. Inflammation of all genes is not the same in the same places. The potential effect of each gene is different in function.
Consider a case of humanoid arthritis. It could be driven by a critical gene, but at the same time, after having a wound or cut, it heals because of the novel function of the impactful Alzheimer’s gene. Whether the Alzheimer’s risk gene causes too much bad or fails to make is need to investigate. Straight looking at the activation inflammation of the gene, we can’t conclude whether its impact will be good or bad, a that’s why further research is required.
By reducing the epileptic activity in mouse one of the inflammation, action is affected that is TREM2 shown by Mucke and his colleagues. TREM 2 is located in the brain’s resident immune cells and is produced by microglia.
The scientists showed TREM2 increase in the brain leads to a decline in epileptic activity. The genetic Variant gene of TREM 2 is likely to cause 2 to 3 times Alzheimer’s disease than normal TREM2. The role of TREM 2 is quite undisclosed as its increase in the brain can bring significant benefits. Several pharmaceutical companies have been established to develop antibodies to enhance the role of TREM 2.
