Deposits in the brain plaques

 A century ago a German doctor called Alice outside spotted anomalies in brain sections from a patient with dementia. Ever since people have been studying the strange plaques and tangles he saw in the hope that we could one day on the stand and kill what is now known outside his disease. Insoluble deposits of a peptide called amyloid-beta A. B. 

 Because the protein is sequentially clean by 2 and beta and gamma-secretase. All the molecules are generated by this cleavage and may play a role in the disease but A. B. tech is the main culprit. ABC tends to miss full become sticky eventually clumping together home saludable all the goodness. Some of these aggregates into large insoluble fibrils the deposits in the brain plaques. 

 We don't know exactly which species is toxic research shows that communication and plasticity. This could be what stops the brain from full. The big memories. New homes on any cells affected outside Missy Esther sites in microglia. Microglia remain cells to clear out waste imprint synopsis during development. Mike could take up a beach. They also get activated by triggering the release of inflammatory cytokines that can damage neurons. Mike Quigley also start to remove synopsis by phagocytosis. 

Another key feature of Alzheimer's disease is neurodegeneration. You are not death and damage is triggered by a beast. Some of a beach's effects seem to be mediated by another scene in the brains of patients town component tangles. In healthy molecules, I carried along with the axon a series of trucks made of microtubules and stabilized by the town. 

Outside his disease turtle is modified causing it to dissociate from the microchip adoption abnormal shape and move from the sun to the cell body. Like a beta, tau comes in a variety of forms we don't know which ones contribute to the disease. I'm like a pizza these films either remain sociable all stick together and deposit the tangles docked outside missile. Eventually, these processes kill. Another problem seen in animal models is that misfolded tau proteins can spread across signed into healthy neurons that make healthy tau proteins start to miss full well spreading knowledge across the bridge. The person is spreading through the different brain regions that match the changing symptoms from early to late stages of Alzheimer's disease. This patent also reflects how sat near a more vulnerable than others to dine. Despite these advances in our understanding of sinus disease no cure exists. What drugs are being developed to target family B. to town it's unclear whether they will eventually be successful in treating the disease. This one second. Continued support for basic and clinical research when enabled us to one day to diagnose and treat this devastating condition. We need deep research further. 

Courtesy: Lecture on Alzheimer's

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