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Common forms of Alzheimer's disease (AD) are complex and polygenic. We have created a research resource that seeks to capture the extremes of polygenic risk in a collection of human induced pluripotent stem cell (iPSC) lines from over 100 donors: the IPMAR Resource (iPSC Platform to Model Alzheimer's Disease Risk). Donors were selected from a large UK cohort of 6,000+ research-diagnosed early or late-onset AD cases and elderly cognitively healthy controls, many of whom have lived through the age of risk for disease development (>85 years). We include iPSC with extremes of global AD polygenic risk (high-risk late-onset AD: 34; high-risk early-onset AD: 29; low-risk control: 27) as well as those reflecting complement pathway-specific genetic risk (high-risk AD: 9; low-risk controls: 10). All iPSC have associated clinical, longitudinal, and genetic datasets and will be available through collaboration or from cell (EBiSC) and data (DPUK) repositories.
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http://dx.doi.org/10.1016/j.stemcr.2025.102570 | DOI Listing |
Elife
September 2025
Human Biology and Primate Evolution, Institute of Biology, Freie Universität Berlin, Berlin, Germany.
Evidence indicates that transposable elements (TEs) can contribute to the evolution of new traits, with some TEs acting as deleterious elements while others are repurposed for beneficial roles in evolution. In mammals, some KRAB-ZNF proteins can serve as a key defense mechanism to repress TEs, offering genomic protection. Notably, the family of KRAB-ZNF genes evolves rapidly and exhibits diverse expression patterns in primate brains, where some TEs, including autonomous LINE-1 and non-autonomous Alu and SVA elements, remain mobile.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psychiatry, Università Campus Bio-Medico di Roma, Roma, Italy.
BackgroundAlzheimer's disease (AD) is the most common neurodegenerative disorder. While AD diagnosis traditionally relies on clinical criteria, recent trends favor a precise biological definition. Existing biomarkers efficiently detect AD pathology but inadequately reflect the extent of cognitive impairment or disease heterogeneity.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Paula Costa-Urrutia Medical Affairs, Terumo BCT, Edificio Think MVD, Montevideo, Uruguay.
BackgroundTherapeutic plasma exchange (TPE) with albumin replacement has emerged as a potential treatment for Alzheimer's disease (AD). The AMBAR trial showed that TPE could slow cognitive and functional decline, along with changes in core and inflammatory biomarkers in cerebrospinal fluid.ObjectiveTo evaluate the safety and effectiveness of TPE in a real-world setting in Argentina.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Department of Community Health and Health Behavior, University at Buffalo, Buffalo, NY, USA.
BackgroundFear of developing Alzheimer's disease and other dementias could motivate defensive responses to dementia information, including public health messaging, and reduce willingness to undergo screening or diagnostic testing for the disease.ObjectiveWe sought to assess the pervasiveness of dementia information avoidance and test whether it is associated with lower willingness to be screened for dementia. We also tested whether lower generalized self-efficacy is associated with higher dementia information avoidance, as the former might be a point of intervention for decreasing defensive information avoidance.
View Article and Find Full Text PDFInflammopharmacology
September 2025
Centre for Research Impact & Outcome, Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India.
The NOD‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a key molecular complex that amplifies inflammatory cascades by maturing interleukin‑1 beta (IL-1β) and interleukin‑18 (IL-18) and inducing pyroptosis. It serves as a major driver and co-driver of numerous diseases associated with chronic inflammation. Dysregulated NLRP3 activation contributes to the progression of disorders such as rheumatoid arthritis, inflammatory bowel disease, neurodegenerative diseases and atherosclerosis.
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