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Reassessing The Cause of Death In Clinical Research | 115058

法医病理学杂志

国际标准期刊号 - 2684-1312

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Reassessing The Cause of Death In Clinical Research

Joanna Grace

The direct examination of brain tissue in people with autism and similar illnesses is made possible by post-mortem investigations. There have been a number of review publications that have concentrated on certain post-mortem anomalies, but none that have compiled all of the post-mortem literature. Here, we conduct a thorough evaluation of the data from post-mortem investigations into autism and other illnesses that exhibit autistic symptoms. A few strikingly consistent conclusions are apparent despite the literature's short number of research and tiny sample sizes. Although there are constant changes in minicolumn numbers and abnormal myelination, cortical layering is essentially unaffected. Transcriptomics frequently links dysfunctional metabolic, apoptotic, proliferation, and immunological processes. Non-coding RNA, abnormal epigenetic profiles, GABAergic, glutamatergic, and glial dysfunction are all implicated in the pathophysiology of autism in sufficient numbers of independent studies. Overall, the frontal cortex and cerebellum are most frequently affected, occasionally showing unique region-specific changes. The body of research on conditions including Fragile X, Rett syndrome, and copy number variants (CNVs) that predispose to autism is extremely thin and contradictory. It is necessary to do larger trials that are matched for gender, developmental stage, co-morbidities, and drug use.

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