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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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Our results provide evidence supporting 25OHD as a causal risk factor for AD.
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Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression.
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Dementia is one of the major causes of disability in later life, and ischemic heart disease is a leading cause of morbidity and mortality.
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Alzheimer's disease (AD) is neuropathologically characterized by neuritic plaques and neurofibrillary tangles.
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Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E ε4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia.
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In this study, serum DHA levels were associated with pathogenesis of cerebral amyloidosis and with preservation of entorhinal and hippocampal volumes.
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Alzheimer's disease (AD) is a gradually debilitating disease that leads to dementia.
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder that causes progressive cognitive decline.
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Efficient intercellular transfer of RNAs, proteins, and lipids as protected exosomal cargo has been demonstrated in the CNS, but distinct physiologic and pathologic roles have not been well defined for this pathway.
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We aimed to identify new candidate genes potentially involved in early-onset Alzheimer's disease (EOAD).
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Proteolysis of the amyloid precursor protein (APP) liberates various fragments including the proposed initiator of Alzheimer disease-associated dysfunctions, amyloid-β.
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Neurodegenerative diseases are distinguished by characteristic protein aggregates initiated by disease-specific 'seed' proteins; however, roles of other co-aggregated proteins remain largely unexplored.
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Genetic risk factors for Alzheimer's disease imply that inflammation plays a causal role in development of the disease.
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The series of events underlying the pathogenesis of Alzheimer disease (AD) in unknown.
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In normal brain, neurons in the cortex and hippocampus produce insulin, which modulates glucose metabolism and cognitive functions.
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Men have a shorter life expectancy compared with women but the underlying factor(s) are not clear.
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Our findings suggest that the proposition that synaptic markers can predict cognitive decline in AD, should be extended to Lewy body diseases.
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This common ABCA7 deletion could represent an ethnic-specific pathogenic alteration in AD.
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ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS).
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55/100
This longitudinal study sought to determine whether the 18 kDa translocator protein (TSPO), a marker of neuroinflammation, increases over time in Alzheimer's disease.
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Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline, such as cardiometabolic diseases.
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55/100
Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD.
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The lack of strong association between brain beta-amyloid deposition and cognitive impairment has been a challenge for the Alzheimer's disease (AD) field.
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Deposition of amyloid-β (Aβ) in the brain parenchyma and vessels is one of the hallmarks of Alzheimer disease (AD).
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Cytoskeletal abnormalities and synaptic loss, typical of both familial and sporadic Alzheimer disease (AD), are induced by diverse stresses such as neuroinflammation, oxidative stress, and energetic stress, each of which may be initiated or enhanced by proinflammatory cytokines or amyloid-β (Aβ) peptides.
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Mitochondrial dysfunction is linked with the etiopathogenesis of Alzheimer disease and Parkinson disease.
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Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02).
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Recent studies highlight the implication of innate and adaptive immunity in the pathophysiology of Alzheimer's disease, and foster immunotherapy as a promising strategy for its treatment.
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There is growing evidence of the involvement of advanced glycation end products (AGEs) in the pathogenesis of neurodegenerative processes including Alzheimer's disease (AD) and their function as a seed for the aggregation of Aβ, a hallmark feature of AD.
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57/100
Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer's disease (AD).
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Neurofibrillary tangles (NFT) and β-amyloid plaques are the neurological hallmarks of both Alzheimer's disease and an unusual paralytic illness suffered by Chamorro villagers on the Pacific island of Guam.
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Alzheimer's disease (AD), the most common form of dementia, is a progressive disorder manifested by gradual memory loss and subsequent impairment in mental and behavioral functions.
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The chemokine/chemokine receptor CCL2/CCR2 axis was impaired in BDMs from AD and MCI patients, causing a deficit in cell migration.
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More research is needed to elucidate the neural mechanisms underlying these regional associations, which may involve motor and sensorimotor circuits hitherto largely neglected in the pathophysiology of AD.
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52/100
Maintaining DNA integrity is vital for all cells and organisms.
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54/100
The genetic variants play a crucial role in the pathogenesis of Alzheimer's disease (AD), while the relationships of specific single nucleotide polymorphisms (SNPs) with AD are still controversial.
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Type 2 diabetes (T2DM), Alzheimer's disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern.
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Biomarkers in the cerebrospinal fluid (CSF) are currently regarded as indispensable indicators for accurate differential diagnosis of neurodegenerative disorders.
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Alzheimer's disease (AD) is characterized by synaptic failure, dendritic and axonal atrophy, neuronal death and progressive loss of cognitive functions.
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Neuroinflammation is a pathological hallmark of Alzheimer's disease (AD), and microglia, the brain's resident phagocyte, are pivotal for the immune response observed in AD.
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Diabetes is a risk factor for Alzheimer disease (AD).
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Crocin, as a carotenoid, is one of the main and active constituents of saffron stigmas (Crocus sativus L.) that is widely used in folk medicine.
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Immune cells of myeloid lineage are encountered in the Alzheimer's disease (AD) brain, where they cluster around amyloid-β plaques.
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We replicated the CLU-MS4A4E interaction in a large case-control series and observed APOE ε4 and possible dominant effect.
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In the past five years, a series of large-scale genetic studies have revealed novel risk factors for Alzheimer's disease (AD).
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To assess the value of exosomal miRNAs as biomarkers for Alzheimer disease (AD), the expression of microRNAs was measured in a plasma fraction enriched in exosomes by differential centrifugation, using Illumina deep sequencing.
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The impact of APOE4 on brain metabolism and structure is modified by sex.
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Amyloid precursor protein (APP) metabolites (amyloid-β (Aβ) peptides) and Tau are the main components of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheimer disease.
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47/100
The ATP-binding cassette transporter A7 (ABCA7) has been identified as a susceptibility factor of late onset Alzheimer disease in genome-wide association studies.
From across this tag
9 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 9. The same 9 appear here every time.
- Increased risk of late posttraumatic seizures associated with inheritance of APOE epsilon4 allele
- The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease
- Genetic Associations with Alzheimer's, Lewy Body and Vascular Neuropathology Reveal Shared and Distinct Biological Pathways
- Whole-genome sequencing reveals new Alzheimer's disease-associated rare variants in loci related to synaptic function and neuronal development
- Proteolytic therapeutic modalities for amyloidoses: Insights into immunotherapy, PROTAC, and photo-oxygenation
- Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory
- Apolipoprotein E, amyloid-beta, and blood-brain barrier permeability in Alzheimer disease
- Fine-mapping of the human leukocyte antigen locus as a risk factor for Alzheimer disease: A case-control study
- Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis?