Choroid plexus genes for CSF production and brain homeostasis are altered in Alzheimer's disease.

摘要: The roles of the choroid plexus (CP) and cerebrospinal fluid (CSF) production have drawn increasing attention in Alzheimer’s disease (AD) research. Specifically, studies document markedly decreased CSF turnover moderate-to-severe AD. Moreover, reduced CP function lead to impaired clearance toxic metabolites, likely promote neuroinflammation, may facilitate neuronal death during AD progression. We analyzed gene expression compared with control subjects, specifically considering those genes involved structural integrity. Brown-Merck Gene Expression Omnibus (GEO) database (CP transcripts) was mined examine changes controls a focus on assorted thought play role production. coding for ion transporters epithelium (CPE) associated enzymes like Na–K-ATPase carbonic anhydrase, aquaporins, mitochondrial transporters/enzymes, blood–cerebrospinal barrier (BCSFB) stability proteins, pro-inflammatory mediators were selected investigation. Data using t test p-value fold-change analysis conducted by GEO2R feature GEO database. Significant several observed CP. These included disruptions (e.g., solute carrier SLC4A5, p = 0.004) enzyme expressions anhydrase CA4, p = 0.0001), along BCSFB integrity claudin CLDN5, p = 0.039) ATP synthesis adenosine triphosphate ATP5L, p = 0.0004). Together all point disrupted transport at blood–CSF interface Increased interleukin IL1RL1, p = 0.00001) potential neurodegenerative amyloid precursor APBA3, p = 0.002) also implicate disturbed function. Because altered numerous transcripts AD-CP help explain AD, these findings represent first step towards identifying novel therapeutic targets