Home › Research › Topics › amyloid-beta
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.
-
53/100
Discovery efforts for susceptibility loci for Alzheimer disease could benefit from the use of neuropathologic intermediate phenotypes as a complement to other approaches.
-
The amyloid precursor protein (APP) is implied both in cell growth and differentiation and in neurodegenerative processes in Alzheimer disease.
-
Oxidative stress has been implicated in the pathogenesis of a number of diseases including Alzheimer's disease (AD).
-
40/100
Retinal ganglion cell loss is considered to be a cause of visual impairment in Alzheimer;s patients.
-
In the oldest old, the presence of the APOE epsilon2 allele (APOE2) was associated with a somewhat reduced risk of dementia, but paradoxically was associated with increased Alzheimer disease (AD) neuropathology.
-
Therapeutic preservation of neuronal PGC-1alpha expression promotes the nonamyloidogenic processing of amyloid precursor protein precluding the generation of amyloidogenic Abeta peptides.
-
Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder.
-
In cerebral amyloid angiopathy (CAA), amyloid fibrils deposit in walls of arteries, arterioles and less frequently in veins and capillaries of the central nervous system, often resulting in secondary degenerative vascular changes.
-
49/100
The epsilon4 allele of APOE is a well-characterized genetic risk factor for late-onset Alzheimer disease (LOAD).
-
The amyloid precursor protein (APP) is cleaved to produce the Alzheimer disease-associated peptide Abeta, but the normal functions of uncleaved APP in the brain are unknown.
-
Alzheimer's disease is a major cause of dementia in humans.
-
Chronic cerebral hypoperfusion (CCH) increases the risk of Alzheimer disease (AD) through several biologically plausible pathways, but the relationship between CCH and the development of AD remains uncertain.
-
49/100
Only Apolipoprotein E polymorphisms have been consistently associated with the risk of late-onset Alzheimer disease (LOAD), but they represent only a minority of the underlying genetic effect.
-
beta-Amyloid (Abeta) deposits are one of the major histopathological hallmarks of Alzheimer's disease (AD).
-
Cholesterol and docosahexenoic acid (DHA) may affect degenerative processes in Alzheimer's Disease (AD) by influencing Abeta metabolism indirectly via the vasculature.
-
Alzheimer disease beta-amyloid (Abeta) peptides are generated via sequential proteolysis of amyloid precursor protein (APP) by BACE1 and gamma-secretase.
-
Amyloid beta-peptide (Abeta) accumulation leads to neurodegeneration and Alzheimer disease; however, amyloid metabolism is a dynamic process and enzymic mechanisms exist for Abeta removal.
-
The antiamnesic and neuroprotective activities of the new aminotetrahydrofuran derivative tetrahydro-N,N-dimethyl-5,5-diphenyl-3-furanmethanamine hydrochloride (ANAVEX1-41), a nonselective muscarinic receptor ligand and sigma1 protein activator, were examined in mice injected intracerebroventricularly with amyloid beta(25-35) (Abeta(25-35)) peptide (9 nmol).
-
Mitochondrial dysfunction is a prominent feature of Alzheimer disease but the underlying mechanism is unclear.
-
One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc).
-
61/100
Although beta-amyloid (Abeta) plaques are a primary diagnostic criterion for Alzheimer's disease, this pathology is commonly observed in the brains of non-demented older individuals.
-
Neurotoxic amyloid beta peptide (Abeta) accumulates in the brains of individuals with Alzheimer disease (AD).
-
MicroRNAs (miRNAs) are key regulatory RNAs known to repress mRNA translation through recognition of specific binding sites located mainly in their 3'-untranslated region (UTR).
-
Uptake of carbon 11-labeled Pittsburgh Compound B ([(11)C]PiB) was measured for participants assessed between August 15, 2003, and January 8, 2008, at the Washington University Alzheimer's Disease Research Center and diagnosed either as nondemented (n = 161) or with dementia of the Alzheimer type (n = 37).
-
There is significant evidence to suggest that a damaged or dysfunctional blood-brain barrier (BBB) may contribute to the pathogenesis of Alzheimer's disease (AD) lesions.
-
Alzheimer's disease (AD) is a terminal age-associated dementia characterized by early synaptic dysfunction and late neurodegeneration.
-
Amyloid precursor protein (APP) mis-processing and aberrant tau hyperphosphorylation are causally related to the pathogenesis and neurodegenerative processes that characterize Alzheimer's disease (AD).
-
Apolipoprotein E (apoE) plays a role in the pathogenesis of Alzheimer disease (AD).
-
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive decline in multiple cognitive domains.
-
57/100
Early microglial accumulation in Alzheimer's disease (AD) delays disease progression by promoting clearance of beta-amyloid (Abeta) before formation of senile plaques.
-
We used a sensitive and specific beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) assay to determine the relationship between BACE1 activity in cerebrospinal fluid (CSF) and markers of APP metabolism and axonal degeneration in early and late stages of Alzheimer disease (AD).
-
Intracellular trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations over the past two decades.
-
Amyloid plaques, composed of the amyloid beta-protein (Abeta), are hallmark neuropathological lesions in Alzheimer disease (AD) brain.
-
Since the discovery of the amyloid precursor protein (APP) in 1987, extensive research has been conducted analyzing the APP-derived beta-amyloid (Abeta) which is found in massive quantities in senile plaques of Alzheimer disease (AD) patients.
-
Astrocyte pathology occurs in association with Alzheimer's disease (AD) and in brain ageing, but is poorly characterised.
-
Researchers extracted soluble amyloid-beta protein oligomers directly from the cerebral cortex of subjects with Alzheimer's disease to study their impact.
-
Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80.
-
Alzheimer's disease is the most common dementia and is pathologically characterized by deposition of amyloid-beta peptide (Abeta) into beta-amyloid plaques, neuronal injury and low-level, chronic activation of brain immunity.
-
Autophagy is the principal cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress.
-
The objective of this study was to analyze factors influencing the risk and timing of Alzheimer's disease (AD) in central Norway.
-
APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease.
-
Inflammation is associated with Abeta pathology in Alzheimer's disease (AD) and transgenic AD models.
-
In this longitudinal study, impaired acute insulin response at midlife was associated with an increased risk of Alzheimer disease (AD) up to 35 years later suggesting a causal link between insulin metabolism and the pathogenesis of AD.
-
58/100
Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors.
-
There is increasing evidence for blood-brain barrier (BBB) compromise in Alzheimer disease (AD).
-
A majority of mutations within the beta-amyloid region of the amyloid precursor protein (APP) gene cause inherited forms of intracerebral hemorrhage.
-
Alzheimer's disease is the commonest dementia.
-
The major molecular risk factor for Alzheimer disease so far identified is the amyloidogenic peptide Abeta(42).
-
50/100
Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult.
-
The risk of dementia and Alzheimer's disease (AD) probably results from an interaction between genetic and environmental factors.
From across this tag
10 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 10. The same 10 appear here every time.
- Age and the association between apolipoprotein E genotype and Alzheimer disease: A cerebrospinal fluid biomarker-based case-control study
- Amyloid-β Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle
- Analysis of European mitochondrial haplogroups with Alzheimer disease risk
- Viral gene transfer of APPsα rescues synaptic failure in an Alzheimer's disease mouse model
- Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model
- Mutations in the Matrin 3 gene cause familial amyotrophic lateral sclerosis
- The cerebral beta-amyloid angiopathies: hereditary and sporadic
- Sex Differences in Neuropathology and Cognitive Behavior in APP/PS1/tau Triple-Transgenic Mouse Model of Alzheimer's Disease
- Distinct regional patterns of synaptic vulnerability across hippocampal and parahippocampal subregions in Alzheimer's disease
- The apolipoprotein epsilon 4 allele in patients with Alzheimer's disease