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amyloid-beta
1,365 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
1,365 studies carry this tag.
Date range
1982 to 2026
Top journals
- Neurology 92
- The Journal of biological chemistry 68
- Proceedings of the National Academy of Sciences of the United States of America 47
- Archives of neurology 43
- JAMA neurology 36
375 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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APP/PS1 mice at 6 months were randomly allocated to two dietary groups: one receiving ad libitum (AL) feeding and the other undergoing IF for 1 month.
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Neural autoantibodies are being increasingly detected in conjunction with neurodegenerative dementias such as Alzheimer's disease dementia (AD), yet their significance is not well clarified.
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Metabolomics provide a promising tool for understanding dementia pathogenesis and identifying novel biomarkers.
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Although the relationship between macroautophagy/autophagy and Alzheimer disease (AD) is widely studied, the underlying mechanisms are poorly understood, especially the regulatory role of the initiation signaling of autophagy on AD.
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-heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens.
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Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear.
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Blood-based biomarkers for Alzheimer's disease (AD) pathology have been investigated intensively as markers for AD-related neurodegeneration.
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However, postmortem investigations indicate that the AD-typical progressive amnestic syndrome may also result from predominantly limbic non-AD neuropathology such as TDP-43 proteinopathy and argyrophilic grain disease.
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We observed differential cellular effects on β-amyloid, pTau217 and cognitive measures.
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Alzheimer?s disease (AD) is a neurodegenerative disorder with a strong genetic component.
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• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD.
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Cerebral small vessel disease can manifest as vascular dementia, typically associated with vascular risk factors or cerebral amyloid angiopathy, and more rarely associated with hereditary conditions.
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Alzheimer's disease (AD), the most common form of dementia, is marked by cognitive decline and amyloid-beta (Aβ) plaque deposition in the brain.
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The rising global prevalence of Alzheimer's disease (AD) and mild cognitive impairment (MCI) underscores the urgent need to elucidate their underlying pathogenic mechanisms.
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• EEG microstate analyses were performed in a cohort of autosomal dominant AD. • Coverage of class C decreased in symptomatic mutation carriers • Coverage of class D decreased in presymptomatic and symptomatic mutation carriers. • Coverage of class E increased in presymptomatic and symptomatic mutation carriers. • The findings may support presymptomatic changes in resting-state neuronal networks.
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APOE ε4 is associated with accelerated progression of AD pathology.
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Alzheimer's disease (AD) is the most common neurodegenerative dementia with multi-layered complexity in its molecular etiology.
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The role of microglia in the amyloid cascade of Alzheimer's disease (AD) is debated due to conflicting findings.
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We observed a relationship between residence in a more disadvantaged neighborhood (higher ADI) and lower rates of amyloid positivity.
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We observed a relationship between residence in a more disadvantaged neighborhood (higher ADI) and lower rates of amyloid positivity.
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Gene therapy to treat hereditary disorders conventionally delivers the normal allele to compensate for loss-of-function mutations.
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Quinoa is an ancient Andean crop with a significant interest due to its nutritional and health benefits.
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MR analysis suggested a causal relationship between decreased blood-derived mtDNA-CN and increased risk of AD (OR = 0.68; P = 0.013).
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This study highlighted that the AD-causal MD genes could be regulated by epigenetic changes and interact with inflammatory cytokines, providing evidence for AD prevention and intervention.
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The strongest risk factors for late-onset sporadic Alzheimer's disease (AD) include the ε4 allele of apolipoprotein E (APOE), the R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2), and female sex.
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61/100
Impaired cerebral glucose metabolism is a pathologic feature of Alzheimer's disease (AD), with recent proteomic studies highlighting disrupted glial metabolism in AD.
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A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses.
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Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective.
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APP gene dosage is strongly associated with Alzheimer's disease (AD) pathogenesis.
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Isolated forebrain synaptosomes, rather than total homogenates, from atg7 iKO mice demonstrated accumulation of synaptic proteins, suggesting that the synapse might be a vulnerable site for protein homeostasis disruption.
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Eighteen years after it was published, Nature formally retracted the landmark 2006 paper that had proposed a specific amyloid protein (Aβ*56) as a cause of memory loss in mice, citing evidence of image manipulation, including splicing, duplication, and use of an image-editing 'eraser' tool.
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Clinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease.
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Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed.
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This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD.
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Analyzing postmortem brain pathology from over 3,200 people plus biomarker data from more than 10,000 more, researchers found that people who inherit two copies of the APOE4 gene variant (about 2-3% of the population) develop Alzheimer's brain changes almost universally and on a predictable timeline starting around age 55, much like known single-gene forms of Alzheimer's. The authors argue this makes APOE4 homozygosity itself a genetic form of Alzheimer's disease rather than just a risk factor.
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Research evidence indicating common metabolic mechanisms through which type 2 diabetes mellitus (T2DM) increases risk of late-onset Alzheimer's dementia (LOAD) has accumulated over recent decades.
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The risk of developing Alzheimer's disease (AD) significantly increases in individuals carrying the APOEε4 allele.
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The authors sought to examine the impact of the K-variant of butyrylcholinesterase (BCHE-K) carrier status on age-at-diagnosis of Alzheimer disease (AD) in APOE4 carriers.
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The Aβ hypothesis has long been central to Alzheimer's disease (AD) theory, with a recent surge in attention following drug approvals targeting Aβ plaque clearance.
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Microglia are central players in Alzheimer's disease pathology but analyzing microglial states in human brain samples is challenging due to genetic diversity, postmortem delay and admixture of pathologies.
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Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele.
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Glymphatic failure may precede amyloid pathology, and predicts amyloid deposition, neurodegeneration, and clinical progression in AD.
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Therapies targeting amyloid, such as monoclonal antibodies like Lecanemab, Aducanumab, and Donanemab, have garnered FDA approval but remain controversial due to limited clinical benefits and significant side effects against Alzheimer.
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The ɛ4 allele of the apolipoprotein E gene (APOE), which translates to the APOE4 isoform, is the strongest genetic risk factor for late-onset Alzheimer disease (AD).
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In mild AD patients aged less than 75 years, the mean age-at-diagnosis of AD in APOE4 carriers was reduced by over 6 years in BCHE-K carriers versus noncarriers.
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Alzheimer's disease (AD) is the most prevalent dementia, affecting a large number of populations.
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Among 68 756 unique individuals, analyses included 21 852 East Asian (demographic data not available), 5738 Hispanic (68.2% female; mean [SD] age, 75.4 [8.8] years), 7145 non-Hispanic Black (hereafter referred to as Black) (70.8% female; mean [SD] age, 78.4 [8.2] years), and 34 021 non-Hispanic White (hereafter referred to as White) (59.3% female; mean [SD] age, 77.0 [9.1] years) individuals.
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67/100
Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female).
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43/100
Macroautophagy/autophagy is the intracellular degradation process of cytoplasmic content and damaged organelles.
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This ITR analysis provides a proof of concept for precision medicine in future AD research and drug development.
From across this tag
9 of the 1,363 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.
- Liver–metabolic stress, apolipoprotein E ε4, and cognition and amyloid burden: findings from the dementia platform Korea trial-ready registry
- Estrogen lowers Alzheimer beta-amyloid generation by stimulating trans-Golgi network vesicle biogenesis
- Phagocytosis and deposition of vascular beta-amyloid in rat brains injected with Alzheimer beta-amyloid
- Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein
- APOE2 is associated with longevity independent of Alzheimer's disease
- Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease
- Mitochondria-associated ER membranes and Alzheimer disease
- Retinal Imaging Findings in Carriers With PSEN1-Associated Early-Onset Familial Alzheimer Disease Before Onset of Cognitive Symptoms
- Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formation