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amyloid-beta
1,346 studies tagged amyloid-beta, dated 1982-09-01 to 2026-10-18. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Evidence for Reduced Somatic T-Cell Receptor Sequence Diversity Profiles Among Midwestern Amish in an Aging Cohort Study 2026-10-18
- Gantenerumab reduces brain amyloid-β proteoforms: Biochemical evaluation in dominantly inherited Alzheimer disease 2026-09-29
- Genetic Insights Into Protective Effects of GLP-1 Receptor Agonists on Stroke and Alzheimer Disease Across Ancestries 2026-09-25
Studies
1,346 studies carry this tag.
Date range
1982 to 2026
Top journals
- Neurology 92
- The Journal of biological chemistry 67
- Proceedings of the National Academy of Sciences of the United States of America 47
- Archives of neurology 43
- JAMA neurology 36
372 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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The causes of late onset Alzheimer disease (LOAD) are not known but several recent lines of evidence implicate the adaptive immune system.
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Symptomatic DIAD participants who had been treated for ∼ 4 years with anti-Aβ monoclonal antibodies (gantenerumab, n=4 or solanezumab, n=4) were compared with untreated, symptomatic DIAD mutation carriers (n=40) and with age-relevant non-DIAD controls with modest or no plaque pathology (n=18).
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Stroke and dementia are leading causes of death and disability worldwide, requiring enhanced preventive strategies.
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INTRODUCTIONInflammation plays a central role in Alzheimers Disease (AD), with oxylipins, endocannabinoids, and polyunsaturated fatty acids (PUFAs) acting as potent modulators.
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Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data.
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INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia.
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder whose genetic architecture and underlying molecular mechanisms remain incompletely understood, particularly in sporadic disease.
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Structured AbstractO_ST_ABSBackgroundC_ST_ABSThe genetic architecture of Alzheimer disease remains incompletely understood.
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Alzheimers disease and related dementias (ADRD)1 and Parkinsons disease and related disorders (PDRD)2 have substantial genetic contributions, yet the role of rare damaging coding variants remains incompletely characterized at population scale3-6.
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ImportanceAnxiety phenotypes - rumination, global anxiety, and worry (RAW) - are increasingly associated with Alzheimers disease and related dementias (ADRD) risk, yet how anxiety phenotypes relate to coordinated, multi-system biology in the at-risk older adults is unknown.
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APOE and PICALM are prominent risk genes for late-onset Alzheimer’s disease (AD).
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 .
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16/100
BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases.
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BackgroundAnti-amyloid-{beta} (A{beta}) monoclonal antibodies are disease-modifying treatments for early Alzheimers disease but are associated with amyloid-related imaging abnormalities (ARIA) and intracranial hemorrhage (ICH).
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ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels.
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BackgroundAlzheimers disease (AD) pathology often accumulates years before memory loss, creating a need to identify high-risk individuals presymptomatically.
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Sex differences in Alzheimers disease (AD) genetic effects and regulatory contexts remain incompletely resolved.
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Brain iron accumulation is well established in Alzheimers disease (AD), but whether the two share a genetic basis remains unclear.
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INTRODUCTIONAPOE*{varepsilon}4 is the strongest genetic risk factor for Alzheimers disease (AD), yet its effect varies across ancestral populations.
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In AβO-injected mice, AR, particularly at 200 mg/kg, attenuated memory deficits, reduced hippocampal neuronal degeneration, preserved synaptic protein immunoreactivity and increased markers of hippocampal cell proliferation and immature neurons.
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38/100
The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease.
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= 0.032). In individuals with LOUE, elevated plasma p-tau217 was associated with both cognitive impairment and disrupted sleep microarchitecture, with the most pronounced cognitive deficits observed in individuals with medication refractory epilepsy.
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The purpose of this meta-analysis was to determine the common signature of dysregulated brain glucose metabolism in late-onset age-associated neurodegenerative diseases (A2NDs), including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis.
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Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease.
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Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear.
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Copy-number variants (CNVs) are major contributors to human disease.
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16/100
Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes.
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Alzheimer disease (AD) pathology affects the transentorhinal/entorhinal region early but whether entorhinal cortex (EC) astrocytes are causal drivers or therapeutic targets remains unresolved.
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Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved.
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16/100
Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood.
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Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus.
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Converging evidence suggests that accumulation may be driven by spreading through network connections and/or interactions with amyloid-β (Aβ).
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These findings suggest that sexual differentiation in early life has modest effects on adult development of AD in females, a relationship that appeared stronger in the context of APOE4 .
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Type 2 diabetes mellitus (T2DM) and major depressive disorder (MDD) are reciprocal risk factors, and both elevate dementia risk.
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43/100
Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4.
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We report the results of structural, functional and genetic studies on the CD33 sialic acid- binding receptor that reveal how non-coding variants in CD33 alter risk for Alzheimer’s disease (AD).
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Sleep spindles (SPs) and slow oscillations (SOs) are linked to cognition and neurodegeneration; however, their relationship with CSF orexin concentrations in symptomatic AD has not been characterized.
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We show that CD33M ectodomain dimerizes, enabling binding of large multi-sialylated molecules.
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32/100
Microglia are central regulators of Alzheimer's disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy.
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To determine the relationship between regional brain edema caused by anti-amyloid monoclonal antibody therapy (ARIA-E) and the degree of regional β-amyloid (Aβ) positron emission tomography (PET) signal reduction.
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Endolysosomal dysfunction has been increasingly implicated in the pathogenesis of neurodegenerative diseases.
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Among 5757 participants (21.7% Black, 20.3% Latinx, 58.1% AORE), we found lower odds of amyloid positivity in Black (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.62-0.83) and Latinx (OR: 0.78, 95% CI: 0.67-0.91) compared to AORE.
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Late-life dementia has a strong heritable component.
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Alzheimer's Disease (AD), the most common form of dementia, is pathologically defined by extracellular beta-amyloid (Aβ) plaques and intraneuronal neurofibrillary tangles (NFTs), accompanied by chronic neuroinflammation.
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The analyses supported stage-dependent remodeling of astrocyte-associated transcriptional and metabolic programs during disease progression.
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The pathological activation of AD microglia significantly amplifies endogenous aging characteristics.
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Among 15,346 White, 829 Latino, 637 Black/African American, and 321 Asian individuals, 51% were female, mean age was 75.7 years, 535 (3.8%) resided in ADI 91 to 100 decile, and 61.6% were amyloid PET positive.
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Alzheimer disease is characterized by gradual and progressive neurodegeneration caused by neuronal cell death.
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Alzheimer’s disease is the leading cause of dementia and represents a growing global health challenge.
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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the deposition of amyloid-β (Aβ) in the walls of leptomeningeal and cortical blood vessels that increases risk of intracerebral hemorrhages and progressive cognitive decline.
From across this tag
9 of the 1,344 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
- Do microglia metabolize fructose in Alzheimer’s disease?
- Deficient brain insulin signalling pathway in Alzheimer's disease and diabetes
- Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study
- Alzheimer’s Disease Risk Gene CD33 Inhibits Microglial Uptake of Amyloid Beta
- Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease
- In silico structure-based multi-targeted molecular docking analysis of ginkgo biloba phytocompounds against Alzheimer’s disease associated proteins
- Melatonin in Alzheimer's Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer's Neuropathology
- Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction
- Clinical features and APOE genotype of pathologically proven early-onset Alzheimer disease