Potential links for common brain disorders that mimic Alzheimer’s disease and its symptoms

Alzheimer’s disease is one of the most common causes of dementia, and although most people may know who is affected by dementia, the genetic factors behind the disease are not well known. Is not … A new study by researchers at Brigham and Women’s Hospital found that Alzheimer’s disease and the major age-related TDP-43 encephalopathy of the limbic system, or common brain disorders that may mimic the recently recognized Alzheimer’s disease. A group of closely related genes has been identified that capture the molecular association between certain LATE symptoms. LATE is often combined with Alzheimer’s disease and causes more rapid cognitive decline. The results of the study Neuron..

“A genetic variation that regulates others gene‘Formulas are believed to play an important role Human illness“However, genome-wide discovery of these mutations was difficult due to the large number of genes and genetic mutations that had to be tested,” said Dr. Philip De Jaguar, Brigham, MD. He is the head of the Department of Neuroimmunology at Columbia University and the lead author of the study. Rather than targeting over 13,000 individual brain-expressed genes.”

Gene expression is the process of assembling proteins using information encoded in genes. The researchers conducted a genome-wide screen of genetic mutations that regulate gene expression using 494 autopsy brain samples from the Religious Order Study (ROS) and the Rush Memory and Aging Project (MAP). Community-based clinicopathologic study of aging and Alzheimer’s disease. They observed that two genes named TMEM106B and RBFOX1 regulate gene expression in the aging brain. The team duplicated the findings in an independent dataset from the Mayo RNAseq study, analyzed clinical, necropsy, and genetic data and associated the findings with dementia-causing brain disease.

The authors note that the study mainly analyzed people with mean ages near death and brain donation near 90 years. Therefore, the findings should be carefully interpreted outside this context, to further investigate whether their findings could be extended to other TDP-43-related conditions affecting young patients such as: Needs further research into Frontotemporal dementia The researchers also found that both amyloid-β accumulation and the TMEM106B risk variant, which are characteristic of Alzheimer’s disease, increase expression of the same set of genes important for lysosomal function. Removal of cellular waste. Next, increased expression of lysosomal genes correlated with LATE neuropathological changes in humans brain..

“It is becoming increasingly clear that the frequent coexistence of Alzheimer’s disease and LATE is not accidental,” said Hyun-Sik Yang, a doctor in cognitive and behavioral neurology at Brigham, the first author of the study. “We need to investigate further the shared molecular link between Alzheimer’s disease and LATE, which one day treats and prevents two of the most common causes of dementia in a rapidly aging population. can.”

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Alzheimer’s disease: new genes may cause early brain changes

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For more information:
Hyun-Sik Yang et al, Genetics of gene expression in the aging human brain reveals the pathophysiology of TDP-43 proteinosis, Neuron (2020). DOI: 10.1016 / j.neuron.2020.05.010

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Brigham and Women’s Hospital

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