Despite the progress in aging research that highlights the role of the nervous system in longevity, whether genes that control development and consequently structure of the nervous system affect lifespan is unclear. We demonstrated that a mutation inshuttle craft, a gene involved in the nervous system development, increased the lifespan of unmated females and decreased the lifespan of mated females, without affecting males. Precise reversions of the mutation lead to the restoration of the lifespan specific to control females. In mutant unmated females, increased lifespan was associated with elevated locomotion at older ages, indicating slowed aging. In mutant mated females, reproduction was decreased compared to controls, indicating a lack of tradeoff between this trait and lifespan. No differences in shuttle craft transcription were observed between whole bodies, ovaries, and brains of mutant and control females of different ages, either unmated or mated. The amount of shuttle craft transcript appeared to be substantially decreased in mutant embryos. Our results demonstrated that a gene that regulates development of the nervous system might also influence longevity, and thus expanded the spectrum of genes involved in lifespan control. We hypothesize that this "carry-over" effect might be the result of transcription regulation in embryos.
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http://dx.doi.org/10.18632/aging.100712 | DOI Listing |
World J Surg Oncol
January 2025
Department of Hepatobiliary Surgery, Guangzhou Red Cross Hospital of Jinan University, Tongfu Roud 396, Guangzhou, 510220, Guangdong, China.
Schwannomas are tumors that originate from the glial cells of the nervous system and can occur on myelinated nerve fibers throughout the body, especially in the craniofacial region. However, pancreatic schwannomas are extremely rare. We report a case of a pancreatic schwannoma that was difficult to differentiate from other pancreatic tumors preoperatively.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
School of Medicine, Chinese PLA General Hospital, Nankai University, Beijing, China.
Background: Glioblastoma multiforme (GBM) exhibits a cellular hierarchy with a subpopulation of stem-like cells known as glioblastoma stem cells (GSCs) that drive tumor growth and contribute to treatment resistance. NAD(H) emerges as a crucial factor influencing GSC maintenance through its involvement in diverse biological processes, including mitochondrial fitness and DNA damage repair. However, how GSCs leverage metabolic adaptation to obtain survival advantage remains elusive.
View Article and Find Full Text PDFNeurol Ther
January 2025
Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy.
Hereditary transthyretin amyloidosis (ATTRv, v for variant) is a genetic disorder characterized by the deposition of misfolded transthyretin (TTR) protein in tissues, resulting in progressive dysfunction of multiple organs, including the nervous system, heart, kidneys, and gastrointestinal (GI) tract. Noninvasive serum biomarkers have become key tools for diagnosing and monitoring ATTRv. This review examines the role of available biomarkers for neurological, cardiac, renal, gastrointestinal, and multisystemic involvement in ATTRv.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
Background: Adenosine deaminase action on RNA 1 (ADAR1) can convert the adenosine in double-stranded RNA (dsRNA) molecules into inosine in a process known as A-to-I RNA editing. ADAR1 regulates gene expression output by interacting with RNA and other proteins; plays important roles in development, including growth; and is linked to innate immunity, tumors, and central nervous system (CNS) diseases.
Results: In recent years, the role of ADAR1 in tumors has been widely discussed, but its role in CNS diseases has not been reviewed.
Mol Psychiatry
January 2025
Institute of Biomedicine, Integrative Physiology and Pharmacology Unit, University of Turku, Turku, Finland.
Childhood maltreatment exposure (CME) increases the risk of adverse long-term health consequences for the exposed individual. Animal studies suggest that CME may also influence the health and behaviour in the next generation offspring through CME-driven epigenetic changes in the germ line. Here we investigated the associated between early life stress on the epigenome of sperm in humans with history of CME.
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