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precursor
1,346 studies tagged precursor, 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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Familial Alzheimer's disease (FAD) is caused by dominant missense mutations in amyloid precursor protein (APP) and presenilin-1 (PSEN1), the catalytic component of γ-secretase that generates amyloid β-peptides (Aβ) from the APP C-terminal fragment C99.
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Longitudinal analysis identified significant associations between the change in ether lipid species (including alkylphosphatidylcholine, alkenylphosphatidylcholine, lysoalkylphosphatidylcholine, and lysoalkenylphosphatidylcholine) and AD dementia conversion.
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Higher AD PRS was associated with increased risks of all-cause dementia (HR: 1.75, 95% CI: 1.70-1.79, P < 0.001) and AD (HR: 2.02, 95% CI: 1.95-2.09, P < 0.001), with stronger effects in women for both outcomes when considering the main AD PRS which was related to APOE4 status.
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Alzheimer's disease (AD) is a neurodegenerative disease, representing the seventh cause of death worldwide and the first cause of dementia.
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It is associated with intracerebral hemorrhage (ICH), cognitive decline, and gait disturbance.
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35/100
Clinical investigations have suggested a potential link between cataracts and Alzheimer's disease (AD).
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We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration.
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Nucleocytoplasmic transport defects are observed in Alzheimer's disease (AD) and frontotemporal dementia (FTD).
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58/100
Of 413 477 All of Us participants, 2038 were eligible.
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The apolipoprotein ε4 allele (APOE4) is associated with decreased longevity and increased vulnerability to age-related declines and disorders across multiple systems.
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Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration.
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Emerging evidence indicates that globus pallidus (GP) function can be modulated by orexin-A in movement disorders, while its role in Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) remains unclear.
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EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification.
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Cross-sectional studies suggest a limited relationship between accelerated epigenetic aging derived from epigenetic clocks, and Alzheimer's disease (AD) pathophysiology or risk.
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16/100
Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E).
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Our results show that genotype, AOF, and sex contributed to AD-like pathology.
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BACKGROUNDTraffic-related air pollution (TRAP) is a risk factor for Alzheimer disease (AD), where unresolved brain inflammation has been linked to deficits in the levels of free lipid mediators that enable the resolution of inflammation.
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Alzheimer's disease (AD) diagnosis relies on cerebrospinal fluid (CSF) biomarkers or amyloid PET.
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value = 0.04). ε4 on cognition is mediated by structural brain imaging markers, driven mainly by cerebral microbleeds.
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Although apolipoprotein E (ApoE) ε4 is a well-established risk factor for Alzheimer disease, its role in the development of post-stroke cognitive impairment (PSCI) remains uncertain.
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Growing evidence highlights sex-related differences in the pathogenesis of Alzheimer's disease (AD).
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Neurodegenerative disorders such as Alzheimer's disease (AD), the most common form of dementia, represent a growing global health crisis, yet current treatment strategies remain primarily palliative.
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Alzheimer's disease (AD) is the most common cause of dementia.
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Biallelic loss-of-function variants in TYROBP and TREM2 cause autosomal recessive presenile dementia with bone cysts known as Nasu-Hakola disease (NHD, alternatively polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, PLOSL).
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Clinical data, animal and cell studies show that some antidiabetic drugs, including glucagon-like peptide 1 receptor agonists (GLP-1RAs), exert therapeutic effects in Alzheimer's disease (AD) via modulation of amyloid-β peptide (Aβ) metabolism.
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APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date.
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• Low ALPS index was significantly associated with high risk of MCI, and the risk of MCI decreased linearly with a higher ALPS index • High ALPS index was dose-dependently associated with a decreased progression from MCI to AD • High ALPS index may delay the MCI onset approximately 3.8 years among CN participants and delay MCI progression to AD by approximately 3.5 years in MCI group • Aβ in choroid plexus, tau in part of the cortex and executive function were partially mediate ALPS-AD association We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors.
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This report highlights a case of relapsing remitting rapidly progressive dementia due to cerebral amyloid angiopathy-related inflammation (CAA-ri), focusing on the diagnostic challenges and the dramatic response to corticosteroid treatment.
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Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups.
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The first search utilized the following MeSH terms and keywords: ‘Plasma Exchange’, ‘Plasmapheresis’, ‘Therapeutic plasma exchange’, ‘Apheresis’, ‘Aβ’, ‘p-tau’, ‘Total-tau’, ‘Alzheimer's disease’, ‘Cognitive dysfunction’, ‘neurodegenerative diseases’, ‘centrifugation’, ‘membranous’, and ‘filtration’ in the Title/Abstract, yielding 146 results.
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Alzheimer's disease (AD) involves a dynamic interaction between neuroinflammation and metabolic dysregulation, where microglia play a central role.
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BackgroundTo date, cholinomimetics remain central in the pharmacotherapy of Alzheimer's disease (AD) dementia.
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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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The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer's disease (AD) cases, is largely unexplained.
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Alzheimer's disease (AD) is an age-associated neurodegenerative disorder with a complex etiology.
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35/100
Alzheimer's disease (AD) is a multifactorial disorder associated with neuroinflammation, elevated oxidative stress, lipid alterations as well as amyloid-deposits and the formation of neurofibrillary tangles.
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Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits.
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65/100
Alzheimer's disease (AD) therapies utilizing amyloid-β (Aβ) immunization have shown potential in clinical trials.
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Age, sex, and apolipoprotein E (APOE) are the strongest risk factors for late-onset Alzheimer disease (AD).
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The CU- group had lower baseline GAP-43 than all Aβ+ groups, but not the other Aβ- groups.
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Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan.
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The amyloid hypothesis is the predominant model of Alzheimer's disease (AD) pathogenesis, suggesting that amyloid beta (Aβ) peptide is the primary driver of neurotoxicity and a cascade of pathological events in the central nervous system.
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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and cognitive decline, with women being disproportionately affected in both prevalence and severity.
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Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis.
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Amyloidoses, which are characterized by abnormal accumulation of amyloid proteins leading to organ dysfunction, represent a major therapeutic challenge.
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H]UCB-J was found to be reduced in frontal cortex from patients with AD.
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We identified that the APOE4 genotype affected ΔHV in females.
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Previous studies have suggested that systemic viral infections may increase risks of dementia.
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Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD).
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Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare.
From across this tag
10 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 10. The same 10 appear here every time.
- Alzheimer's disease phenotypes and genotypes associated with mutations in presenilin 2
- ATP-binding cassette transporter A7 (ABCA7) loss of function alters Alzheimer amyloid processing
- Mapping sex differences in brain and cognition in relation to APOE ε4 and amyloid burden: A longitudinal normative modelling study
- Association Between Choroid Plexus Morphological Alterations, Alzheimer Pathologies, and Cognitive Impairment
- Regulatory T cells delay disease progression in Alzheimer-like pathology
- Homocysteine exacerbates β-amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles
- Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease
- Decreased Prevalence of Alzheimer Disease Associated With 3-Hydroxy-3-Methyglutaryl Coenzyme A Reductase Inhibitors
- Co-expression patterns of microglia markers Iba1, TMEM119 and P2RY12 in Alzheimer's disease
- Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer's disease