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.
-
Interaction of the amino- and carboxyl-terminal domains in apolipoprotein (apo) E, referred to as domain interaction, is predicted to be more pronounced in apoE4 than in apoE3 and to underlie the association of apoE4 with Alzheimer and cardiovascular diseases.
-
41/100
Transmembrane proteins BRI2 and amyloid precursor protein (APP) co-localize with amyloid beta (Abeta) lesions in sporadic Alzheimer disease and mutations in both precursor proteins are linked to early-onset familial cases of cerebral amyloidosis associated with dementia and/or cerebral hemorrhage.
-
Amyloid-beta peptide is elevated in the brains of patients with Alzheimer disease and is believed to be causative in the disease process.
-
Synaptic dysfunction is one of the earliest events in the pathogenesis of Alzheimer disease (AD).
-
Previous studies show increased levels of lipid peroxidation and neurotoxic by-products of lipid peroxidation including 4-hydroxynonenal (HNE) and acrolein in vulnerable regions of the Alzheimer's disease (AD) brain.
-
Alzheimer disease (AD), the most common senile dementia, is characterized by amyloid plaques, vascular amyloid, neurofibrillary tangles, and progressive neurodegeneration.
-
Alzheimer disease (AD) is characterized neuropathologically by intracellular neurofibrillary tangles (NFT) and of extracellular senile plaques (SP), the central core of which is amyloid beta-peptide (Abeta) derived from amyloid precursor protein (APP), a transmembrane protein.
-
Patients with Alzheimer's disease (AD) have abnormally low positron emission tomography (PET) measurements of the cerebral metabolic rate for glucose (CMRgl) in regions of the precuneus and the posterior cingulate, parietotemporal, and frontal cortex.
-
Alzheimer's disease, the most common neurodegenerative disorder of senile dementia, is characterized by two major morpho-pathological hallmarks.
-
APOE epsilon4 carrier status was associated with conversion to AD in older outpatients after controlling for known demographic and clinical risk factors, and APOE epsilon4 homozygosity was associated with increased risk of conversion to AD.
-
61/100
This observational study provides further evidence that lipid-lowering agents are associated with decreased risk of dementia, whereas hyperlipidemia is associated with increased odds for non-Alzheimer-disease-type dementia.
-
49/100
Epidemiological studies suggest that individuals with greater education or more cognitively demanding occupations have diminished risk of developing dementia.
-
Microglia accumulation at the site of amyloid plaques is a strong indication that microglia play a major role in Alzheimer's disease pathogenesis.
-
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), or Nasu-Hakola disease, is a presenile dementia associated with loss of myelin, basal ganglia calcification, and bone cysts.
-
We determined whether oxidative stress is an early event in the pathogenesis of sporadic Alzheimer disease (AD), and correlated oxidative stress with neuropsychological functions and neurofibrillary pathology in AD and mild cognitive impairment (MCI).
-
Transgenic mice made by crossing animals expressing mutant amyloid precursor protein (APPswe) to mutant presenilin 1 (PS1dE9) allow for incremental increases in Abeta42 production and provide a model of Alzheimer-type amyloidosis.
-
Diverse oxidative pathways, such as direct oxidation of amino acids, glycoxidation, and lipoxidation could contribute to Alzheimer disease pathogenesis.
-
Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7).
-
Epidemiological studies suggest that increased intake of the omega-3 (n-3) polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) is associated with reduced risk of Alzheimer's disease (AD).
-
The role of microglia recruited from bone marrow (BM) into the CNS during the progression of Alzheimer's disease (AD) is poorly understood.
-
50/100
The results suggest that brain response differences are not due to poorer general memory abilities, differential atrophy, or brain response during control conditions, but instead appear to be directly influenced by APOE genotype.
-
Recent evidence suggests that statin use may be associated with a decreased risk for Alzheimer disease, although the mechanisms underlying this apparent risk reduction are poorly understood.
-
A generally similar pattern of cerebral hypometabolism was detected in APOE epsilon4-positive and -negative patients with Alzheimer disease.
-
Neuropsychiatric symptoms seen in Alzheimer's disease (AD) are not simply a consequence of neurodegeneration, but probably result from differential neurotransmitter alterations, which some patients are more at risk of than others.
-
40/100
It is generally accepted that human Alzheimer's disease (AD) neuropathology markers are completely absent in rodent brains.
-
After 1 year, 8 of 37 patients with MCI converted to AD (22%).
-
Dietary influences on Alzheimer disease (AD) are gaining recognition.
-
The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood.
-
Oxidative stress is extensive in Alzheimer disease (AD) brain.
-
Inhaled anesthetics enhance oligomerization and cytotoxicity of Alzheimer disease-associated peptides.
-
Mutations in presenilins (PS) 1 and 2 are the major cause of familial Alzheimer's disease.
-
Myeloperoxidase, a heme protein expressed by professional phagocytic cells, generates an array of oxidants which are proposed to contribute to tissue damage during inflammation.
-
The neuronal lysosomal system is a major degradative pathway, induced by cell stress and closely linked to Alzheimer disease (AD) and other neurodegenerative diseases.
-
We examined the association of mtDNA variation with Alzheimer disease (AD) risk in Caucasians (989 cases and 328 controls) testing the effect of individual haplogroups and single nucleotide polymorphisms (SNPs).
-
42/100
We compared lesions in elderly transgenic (tg) mice carrying the Swedish double mutation KM670/671NL with lesions in Alzheimer disease (AD) by histochemical and immunohistochemical techniques.
-
We have previously shown that apolipoprotein E (Apoe) promotes the formation of amyloid in brain and that astrocyte-specific expression of APOE markedly affects the deposition of amyloid-beta peptides (Abeta) in a mouse model of Alzheimer disease.
-
Neuropathological changes generated by human amyloid-beta peptide (Abeta) fibrils and Abeta-acetylcholinesterase (Abeta-AChE) complexes were compared in rat hippocampus in vivo.
-
Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease.
-
The epsilon4 allele of APOE is a risk factor for Alzheimer disease (AD).
-
The APOE-4 allele increases risk and decreases age at onset of PD, an association that may not be dependent upon cognitive impairment.
-
The epsilon4 allele does not predict cholinergic decline in AD.
-
61/100
Memory declined in APOE e4 carriers before the symptomatic presentation of MCI in a cohort whose mean age was 60 years over a median period of 33 months.
-
A change of the prion protein conformation results in a class of neurodegenerative diseases called the transmissible spongiform encephalopathies (like mad cow and Creutzfeld-Jakob diseases).
-
Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT).
-
In Alzheimer disease (AD) patients, early memory dysfunction is associated with glucose hypometabolism and neuronal loss in the hippocampus.
-
The extracellular accumulation of amyloid-beta (Abeta) in neuritic plaques is one of the characteristic hallmarks of Alzheimer's disease (AD), a progressive dementing neurodegenerative disorder of the elderly.
-
The APOE epsilon4 allele acts as a potent risk factor for AD by accelerating onset.
-
Amyloid plaques appear early during Alzheimer's disease (AD), and their development is intimately linked to activated astrocytes and microglia.
-
Synaptic damage and loss are factors that affect the degree of dementia experienced in Alzheimer disease (AD) patients.
-
Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques.
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.
- Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis
- Comparative profiling of cortical gene expression in Alzheimer's disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation
- Proteolytic processing and cell biological functions of the amyloid precursor protein
- ATG5 (autophagy related 5) in microglia controls hippocampal neurogenesis in Alzheimer disease
- The Novel Role of PPAR Alpha in the Brain: Promising Target in Therapy of Alzheimer's Disease and Other Neurodegenerative Disorders
- Contribution to Alzheimer's disease risk of rare variants in TREM2, SORL1, and ABCA7 in 1779 cases and 1273 controls
- Clinicopathologic and 11C-Pittsburgh compound B implications of Thal amyloid phase across the Alzheimer's disease spectrum
- Alzheimer precursor protein interaction with the Nogo-66 receptor reduces amyloid-beta plaque deposition
- Amyloid beta: multiple mechanisms of toxicity and only some protective effects?
- Role of apolipoprotein E (ApoE) ε4 in cognitive impairment after a stroke: a prospective cohort study