Publications by authors named "Bailey Rawlinson"
Background: Progressive supranuclear palsy (PSP) is a neurodegenerative disorder involving pathological deposition of tau that includes glial inclusions and specific regional vulnerability patterns. Therapeutic developments are hampered by incomplete understanding of disease mechanisms. Few studies have examined its cell type-specific effects.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is characterized by the presence of neurofibrillary tangles made of hyperphosphorylated tau and senile plaques composed of beta-amyloid. These pathognomonic deposits have been implicated in the pathogenesis, although the molecular mechanisms and consequences remain undetermined. UFM1 is an important, but understudied ubiquitin-like protein that is covalently attached to substrates.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is characterized by the presence of neurofibrillary tangles made of hyperphosphorylated tau and senile plaques composed of beta-amyloid. These pathognomonic deposits have been implicated in the pathogenesis, although the molecular mechanisms and consequences remain undetermined. UFM1 is an important, but understudied ubiquitin-like protein that is covalently attached to substrates.
View Article and Find Full Text PDFArticle Synopsis
- The letter discusses how new types of cryptic proteins produced by TDP-43 dysfunction could indicate TDP-43-related issues in neurodegenerative diseases.
- It highlights the significance of these novel proteins as potential biomarkers for diagnosing or understanding these diseases.
- The findings could lead to improved methods for detecting and studying conditions linked to TDP-43 pathology, such as ALS and frontotemporal dementia.
Article Synopsis
- Genetic variation in the TMEM106B gene is linked to the risk and progression of frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP), with a specific genotype (rs3173615) associated with longer survival after symptoms begin.
- Research shows that the protective genotype is linked to lower accumulation of TMEM106B filaments, while the risk allele correlates with increased TMEM106B core deposition and enhanced TDP-43 dysfunction.
- The findings indicate that managing the accumulation of TMEM106B filaments may be a crucial factor in reducing disease risk and slowing down the progression of FTLD-TDP.
Article Synopsis
- * Researchers analyzed 192 post-mortem brains to identify the accumulation of cryptic RNAs associated with TDP-43 dysfunction, finding significant presence in the amygdala and hippocampus of AD-TDP cases.
- * The findings propose that these cryptic RNAs could serve as valuable diagnostic and therapeutic targets for AD, indicating a potential shared molecular mechanism between AD-TDP and other neurodegenerative conditions like frontotemporal lobar degeneration (FTLD-TDP).