There is a new say about the mechanism of alzheimer's disease

research and clinical intervention in the academic journal Alzheimer's disease and dementia has published the research results of Professor Han Hongbin's team at Peking University's Third Hospital in the form of a featured article. The study found that the accumulation of A-beta amyloid, a key protein that induces dementia, can lead to blockages in the surrounding microenve environment necessary for the survival of neurons in the brain, and proposed a new hypothesis that A-beta clogging cell gaps induce dementia, providing new ideas and methods for clinical treatment of dementia.
Han Hongbin introduced that due to the lack of lymphatic system in the brain, the drain of its tissue fluid depends on the transfer of substances in the cell gap to achieve, which is to maintain the cerebral microennial stability guarantee. In order to study the structure of cell gap in a wide area deep in the brain, the law of material transport within it, and the changes in the occurrence of dementia, Han Hongbin's team developed a new magnetic trace imaging method, which successfully showed the drainage of deep tissue fluid in the brain.
Although the level of alzheimer's spots aggregated by A-beta is not directly related to the degree of dementia, the high concentration of A-beta induced by mutations in the APP (A-beta prebiogen) gene is still recognized as the key cause of inherited dementia, said Tong Zhixuan, co-author of the paper and an associate researcher at the Beijing Institute of Major Brain Diseases. Unfortunately, although scientists know that A-beta amyloid is a key pathological feature of dementia, antibodies, vaccines, and small molecule compounds produced, aggregated, and purged by A-beta have not achieved the expected clinical results for decades. The biological behavior of A-beta amyloid in and outside cells, including positioning and how to induce dementia, remains an unsolt mystery.
Han Hongbin team through magnetic tracer imaging technology found that: A beta amyloid protein aggregation can lead to the survival of brain neurons necessary for the surrounding microenve environment blockage, induced by the cell gap in the lymphatic fluid flow difficulties, resulting in nutrients, metabolic waste, neurotransmitters, hormones and so on can not be successfully exchanged around the cell, play their due functions, resulting in the death of deep sea horse neurons, space memory loss. The study also confirmed that the use of nano-red light to crush elderly spots deposited in the brain from A-beta can again unblock the extracellular gap and restore the flow of intercellular fluid to save damaged memories.
(Health Journal)