Alzheimer's disease has been identified as a protein misfolding disease (proteopathy), caused by plaque accumulation of abnormally folded amyloid beta protein and tau protein in the brain. But when these tangles start to misfold, it leads to abnormal aggregates of tau proteins causing Alzheimer's disease. These protein-rich … PubMed. Nature. Tau protein promotes assembly and stabilizes microtubules, which contributes to the proper function of neuron. These proteins are in everyone’s brains – tau proteins. Tau has long been a prime suspect in the search for the cause of Alzheimer's disease. A specific form of the tau protein, called phosphorylated-tau-217 or p-tau217, may function as a blood biomarker of Alzheimer’s disease, allow the development of blood tests to accurately diagnose the disease at earlier stages. 1996 Oct 10;383(6600):550-3. Alzheimer's disease (AD) is the most common type of dementia. These are the hallmarks of Alzheimer’s, and they drive the disease’s infamous symptoms, like memory loss, behavioral issues and problems thinking. 2015; S6: 005 Lara Hvidsten,et al. This comes from new research presented at the Alzheimer’s Association International Conference this week, and suggests that treatments for Alzheimer’s may need to differ by gender. Abnormal tau protein may also be in the cerebrospinal fluid that circulates and cushions the brain and spinal cord. First, let’s take a look at one of the main causes of Alzheimer’s disease: tau protein tangles. Loss of memory that affects daily life—forgetting information that was recently learned. 50 million people worldwide are living with Alzheimer’s disease or some form of dementia. The tau tangles generally accumulate in our brains as we age. Changes in brain chemistry make tau protein molecules come away from the microtubules and stick to each other instead. The endosomal pathway is responsible for the secretion of proteins after cleavage, and defective endosomal pathway contributes to AD pathogenesis. Mar. The majority of the damage comes from two specific proteins, beta-amyloid and tau. One of the hallmarks of Alzheimer’s disease is the so-called tau tangles. MTBR-tau species enriched in Alzheimer’s disease brain (MTBR-tau-243, MTBR-tau-299, and MTBR-tau-354) were significantly increased over time in the amyloid-positive group (P < 0.01 by two-tailed paired t-test between first and second visits) but not the amyloid-negative group, except for MTBR-tau-243 (Supplementary Fig. The tests may be done along with cognitive tests and brain scans when an individual has signs and symptoms of Alzheimer disease, such as:. The microtubule-associated protein tau (MAPT) is abnormally deposited as intracellular, filamentous aggregates in a family of neurodegenerative diseases termed tauopathies—a group that includes Alzheimer disease, progressive supranuclear palsy, corticobasal degeneration, and Pick disease. In connection with the global trend of prolonging human life and the increasing number of elderly in the population, the AD becomes one of the most serious health and socioeconomic problems of the present. Tau tangles and beta-amyloid plaques — large accumulations of microscopic brain protein fragments that scientists believe contribute to the slowing of a person’s ability to think and remember — are hallmarks of Alzheimer’s disease. While some scientists are focused on targeting beta-amyloid plaques to treat Alzheimer’s, others are honing in on another hallmark of the disease — pathological tau proteins — and developing a tau vaccine in hopes of preventing the disease. 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