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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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Alzheimer's disease (AD) is the most common cause of dementia in developed countries.
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MicroRNAs (miRNAs) are small regulatory RNAs that participate in posttranscriptional gene regulation in a sequence-specific manner.
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62/100
Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE.
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Alzheimer disease amyloid beta-peptide (Abeta) is generated via proteolytic processing of the beta-amyloid precursor protein by beta- and gamma-secretase.
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Of 214 participants, 48 showed no decline on any test, 126 showed decline on only 1 test in 1 or more domains, and 40 showed decline on 2 or more tests in 1 or more domains.
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Accumulating evidence suggests insulin and insulin signaling may be involved in the pathophysiology of Alzheimer disease (AD).
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Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed in brain tissue from AD patients.
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Alzheimer disease is a common age-related neurodegenerative disease characterized pathologically by senile plaques, neurofibrillary tangles, synaptic disruption, and progressive neuronal deficits.
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Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD).
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In a previous study, we found that human neural stem cells (HNSCs) exposed to high concentrations of secreted amyloid-precursor protein (sAPP) in vitro differentiated into mainly astrocytes, suggesting that pathological alterations in APP processing during neurodegenerative conditions such as Alzheimer's disease (AD) may prevent neuronal differentiation of HNSCs.
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The aspartyl protease beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) initiates processing of amyloid precursor protein (APP) into amyloid beta (Abeta) peptide, the major component of Alzheimer disease (AD) plaques.
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High dietary cholesterol and low dietary docosahexaenoic acid (DHA) intake are risk factors for Alzheimer's disease (AD).
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Mutation of the amyloid precursor protein (APP), presenilin-1, or presenilin-2 results in the development of early onset autosomal dominant forms of Alzheimer disease (AD).
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45/100
The amino acid sequence of amyloid precursor protein (APP) is highly conserved, and age-related A beta aggregates have been described in a variety of vertebrate animals, with the notable exception of mice and rats.
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Many proteins suspected of causing neurodegenerative diseases exist in diverse assembly states.
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The SPM analysis showed that patients with MCI had significantly higher [(11)C]PIB uptake vs control subjects in the frontal, parietal, and lateral temporal cortices as well as in the posterior cingulate showing the most prominent differences.
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These results strongly support the concept that synapse loss is a structural correlate involved very early in cognitive decline in mild Alzheimer disease (mAD) and supports mild cognitive impairment as a transitional stage between mAD and no cognitive impairment.
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Amyloid precursor protein (APP) metabolism is central to the pathogenesis of Alzheimer disease.
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The epsilon(4) allele of APOE confers a two- to fourfold increased risk for late-onset Alzheimer's disease (LOAD), but LOAD pathology does not all fit neatly around APOE.
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45/100
Mutations in presenilins are responsible for approximately 40% of all early-onset familial Alzheimer disease (FAD) cases in which a genetic cause has been identified.
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Selective increases in soluble Abeta(1-42) after TBI may predispose individuals with a brain injury to Alzheimer disease pathology.
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Alzheimer disease (AD) includes inflammatory processes in the senile plaques and surrounding glia, with increased expression of acute phase proteins such as C-reactive protein (CRP) and IL-6.
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This study confirms the association between genetic variants in SORL1 and AD.
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Microglia are the principal immune cells of the brain.
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A number of studies reported that oxidative and nitrosative damage may be important in the pathogenesis of Alzheimer's disease (AD).
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The plasma Abeta42/Abeta40 ratio may be a useful premorbid biomarker for identifying cognitively normal elderly white subjects who are at increased risk for developing MCI or AD.
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Advanced age and presence of intracerebral amyloid deposits are known to be major risk factors for development of neurodegeneration in Alzheimer's disease (AD), and both have been associated with microglial activation.
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46/100
Microglia are the main immune cells of the brain, and under some circumstances they can play an important role in removal of fibrillar Alzheimer amyloid beta peptide (fAbeta).
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Identification of preclinical markers is required for early diagnosis of Alzheimer's disease (AD) and cognitive dysfunction in advancing age.
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The somatodendritic accumulation of hyperphosphorylated tau proteins is an early event preceding the appearance of neurofibrillary tangles (NFT) in Alzheimer's disease (AD) and might be necessary for their formation.
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Presenilin mutations are the main cause of familial Alzheimer disease.
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53/100
This article discusses how distinct protein aggregates found in various neurodegenerative disorders appear to cause these conditions.
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Amyloid beta (Abeta) immunoreactivity in neurons was examined in brains of 32 control subjects, 31 people with Down syndrome, and 36 patients with sporadic Alzheimer's disease to determine if intraneuronal Abeta immunoreactivity is an early manifestation of Alzheimer-type pathology leading to fibrillar plaque formation and/or neurofibrillary degeneration.
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61/100
The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease.
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Microglial activation is a key feature in Alzheimer's disease and is considered to contribute to progressive neuronal injury by release of neurotoxic products.
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Amyloid-beta (Abeta) toxicity has been postulated to initiate synaptic loss and subsequent neuronal degeneration seen in Alzheimer's disease (AD).
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40/100
A small, orally available natural product penetrates into the brain in vivo to rescue the memory impairment produced by soluble Abeta oligomers through a mechanism that restores hippocampal synaptic plasticity.
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Alzheimer's disease is the most common cause of dementia in the elderly, and manifests as progressive cognitive decline and profound neuronal loss.
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Amyloidogenic processing of the amyloid precursor protein (APP) results in the generation of beta-amyloid, the main constituent of Alzheimer plaques, and the APP intracellular domain (AICD).
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Alzheimer's disease (AD), the leading cause of dementia, involves regionalized neuronal death, synaptic loss, and an accumulation of intraneuronal, neurofibrillary tangles and extracellular senile plaques.
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Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy.
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Mutations in the genes for amyloid precursor protein (APP) and presenilins (PS1, PS2) increase production of beta-amyloid 42 (Abeta42) and cause familial Alzheimer's disease (FAD).
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Previous studies have described altered expression of metallothioneins (MTs) in neurodegenerative diseases like multiple sclerosis (MS), Down syndrome, and Alzheimer's disease (AD).
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Neprilysin (NEP) degrades amyloid-beta (Abeta) and is thought to contribute to its clearance from the brain.
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38/100
Affibody (Affibody) ligands specific for human amyloid beta (Abeta) peptides (40 or 42 amino acid residues in size), involved in the progress of Alzheimer's disease, were selected by phage display technology from a combinatorial protein library based on the 58-amino acid residue staphylococcal protein A-derived Z domain.
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These results may lead to a new avenue of inquiry in the prevention of Alzheimer's disease.
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45/100
LR11 is an ApoE receptor that is enriched in the brain.
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We assessed the impact of amyloid precursor protein (APP) gene locus duplications in early onset Alzheimer's disease in a Dutch population-based sample.
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We hypothesized that telomere length might thus relate to increased risk for dementia and mortality.
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These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition.
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.
- Cerebral amyloid angiopathy and Alzheimer disease - one peptide, two pathways
- Sex Differences in Apolipoprotein E and Alzheimer Disease Pathology Across Ancestries
- A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation
- Rare variants in APP, PSEN1 and PSEN2 increase risk for AD in late-onset Alzheimer's disease families
- Relationship of microglia and astrocytes to amyloid deposits of Alzheimer disease
- Amyloid-β and tau: the trigger and bullet in Alzheimer disease pathogenesis
- Processing of Alzheimer beta/A4 amyloid precursor protein: modulation by agents that regulate protein phosphorylation
- Endogenous estrogen levels and Alzheimer's disease among postmenopausal women
- Identification of the Alzheimer beta/A4 amyloid precursor protein in clathrin-coated vesicles purified from PC12 cells
- Increased Plasma Beta-Secretase 1 May Predict Conversion to Alzheimer's Disease Dementia in Individuals With Mild Cognitive Impairment