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Author Correction: Global potential for natural regeneration in deforested tropical regions
Publisher Correction: Spatially restricted immune and microbiota-driven adaptation of the gut
More-powerful AI is coming. Academia and industry must oversee it — together
Loose ends
A science mega-programme is taking shape in the EU: what it means for researchers
Andrew V. Schally obituary: Nobel prizewinner who transformed cancer therapies with research into brain hormones
Mapping the microRNA landscape in the older adult brain and its genetic contribution to neuropsychiatric conditions
Wuhan lab samples hold no close relatives to virus behind COVID
Imperfect wound healing sets the stage for chronic diseases
Science, Volume 386, Issue 6726, December 2024.
Dissecting the hydrogen bond network of water: Charge transfer and nuclear quantum effects
Science, Volume 386, Issue 6726, December 2024.
Ecological erosion and expanding extinction risk of sharks and rays
Science, Volume 386, Issue 6726, December 2024.
Engineering synthetic suppressor T cells that execute locally targeted immunoprotective programs
Science, Volume 386, Issue 6726, December 2024.
Programming tissue-sensing T cells that deliver therapies to the brain
Science, Volume 386, Issue 6726, December 2024.
Amid cuts to basic research, New Zealand scraps all support for social sciences
Scientists shocked as “blue-sky” Marsden Fund has half its budget shifted to research focused on helping economy
Notre Dame’s spectacular rebirth offers bounty of data for scientists
Studies of materials salvaged from 2019 fire are providing insights into everything from construction techniques to climate conditions in medieval France
Genetic risk factors for late-onset Alzheimer's disease drive senescence in female tauopathy mice
Carling et al. report that late-onset Alzheimer's disease (LOAD) risk alleles drive cellular senescence, a hallmark of aging, in a tau- and sex-dependent manner. Mechanistic insights into interactions among genetic risk, biological aging, and sex differences in LOAD are presented.
Apolipoprotein E aggregation in microglia initiates Alzheimer's disease pathology by seeding beta-amyloidosis
No abstract
Deciphering proteins in Alzheimer's disease: A new Mendelian randomization method integrated with AlphaFold3 for 3D structure prediction
Hidden confounding biases hinder identifying causal protein biomarkers for Alzheimer's disease in non-randomized studies. While Mendelian randomization (MR) can mitigate these biases using protein quantitative trait loci (pQTLs) as instrumental variables, some pQTLs violate core assumptions, leading to biased conclusions. To address this, we propose MR-SPI, a novel MR method that selects valid pQTL instruments using Leo Tolstoy's Anna Karenina principle and performs robust post-selection...
Monoclonal therapy with lecanemab in the treatment of mild Alzheimer's disease: A systematic review and meta-analysis
Alzheimer's disease, a progressive neurodegenerative pathology, is characterized by the accumulation of Amyloid-β plaques in the brain. Lecanemab (BAN2401), a humanized IgG1 monoclonal antibody, binds with high affinity to Amyloid-β protofibrils. It is the first monoclonal antibody for Alzheimer's disease to receive full FDA approval. This systematic review, conducted meticulously, examines the current use and safety of Lecanemab in treating Alzheimer's disease. We screened literature from...
Multifaceted roles of DLG3/SAP102 in neurophysiology, neurological disorders and tumorigenesis
DLG3, also known as Synapse-associated protein 102 (SAP102), is essential for the organization and plasticity of excitatory synapses within the central nervous system (CNS). It plays a critical role in clustering and moving key components necessary for learning and memory processes. Mutations in the DLG3 gene, which result in truncated SAP102 proteins, have been associated with a range of neurological disorders, including X-linked intellectual disability (XLID), autism spectrum disorders (ASD),...