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apolipoprotein
1,613 studies tagged apolipoprotein, dated 1982-09-01 to 2026-10-27. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
1,613 studies carry this tag.
Date range
1982 to 2026
Top journals
- Neurology 93
- The Journal of biological chemistry 68
- Proceedings of the National Academy of Sciences of the United States of America 52
- Archives of neurology 43
- Neurobiology of aging 38
457 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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N-Terminally truncated and pyroglutamate (pGlu) modified amyloid beta (Abeta) peptides are major constituents of amyloid deposits in sporadic and inherited Alzheimer's disease (AD).
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The neurotrophin, brain-derived neurotrophic factor (BDNF), is essential for synaptic function, plasticity and neuronal survival.
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Recent evidence has suggested a role for soluble oligomeric Abeta species in the pathology of Alzheimer's disease (AD).
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55/100
The brain changes associated with AD may already begin developing early in middle age, especially among APOE epsilon 4 carriers.
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Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive impairment (MCI) and late-stage Alzheimer's disease (AD).
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Fibrillar amyloid-beta (Abeta) is found in the brains of many cognitively normal older people.
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54/100
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These results indicate that the epsilon4-positive APOE genotype not only represents a risk factor for Alzheimer disease (AD), but also results in higher levels of Abeta plaque deposition in epsilon4-positive patients with AD compared to age-matched epsilon4-negative patients with similar levels of cognitive impairment and brain atrophy.
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We recently surveyed the relationship between the human brain transcriptome and genome in a series of neuropathologically normal postmortem samples.
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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.
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The amyloid precursor protein (APP) is implied both in cell growth and differentiation and in neurodegenerative processes in Alzheimer disease.
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Oxidative stress has been implicated in the pathogenesis of a number of diseases including Alzheimer's disease (AD).
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40/100
Retinal ganglion cell loss is considered to be a cause of visual impairment in Alzheimer;s patients.
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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.
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Therapeutic preservation of neuronal PGC-1alpha expression promotes the nonamyloidogenic processing of amyloid precursor protein precluding the generation of amyloidogenic Abeta peptides.
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Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder.
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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.
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49/100
The epsilon4 allele of APOE is a well-characterized genetic risk factor for late-onset Alzheimer disease (LOAD).
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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.
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Alzheimer's disease is a major cause of dementia in humans.
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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.
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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.
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beta-Amyloid (Abeta) deposits are one of the major histopathological hallmarks of Alzheimer's disease (AD).
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36/100
Apolipoprotein (apo) E has roles beyond lipoprotein metabolism.
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Cholesterol and docosahexenoic acid (DHA) may affect degenerative processes in Alzheimer's Disease (AD) by influencing Abeta metabolism indirectly via the vasculature.
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Alzheimer disease beta-amyloid (Abeta) peptides are generated via sequential proteolysis of amyloid precursor protein (APP) by BACE1 and gamma-secretase.
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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.
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Mitochondrial dysfunction is a prominent feature of Alzheimer disease but the underlying mechanism is unclear.
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One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc).
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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.
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Neurotoxic amyloid beta peptide (Abeta) accumulates in the brains of individuals with Alzheimer disease (AD).
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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).
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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).
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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.
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The genetic underpinnings of Alzheimer's disease (AD) remain largely elusive despite early successes in identifying three genes that cause early-onset familial AD (those that encode amyloid precursor protein (APP) and the presenilins (PSEN1 and PSEN2)), and one genetic risk factor for late-onset AD (the gene that encodes apolipoprotein E (APOE)).
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Alzheimer's disease (AD) is a terminal age-associated dementia characterized by early synaptic dysfunction and late neurodegeneration.
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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).
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Apolipoprotein E (apoE) plays a role in the pathogenesis of Alzheimer disease (AD).
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive decline in multiple cognitive domains.
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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.
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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).
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Intracellular trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations over the past two decades.
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Amyloid plaques, composed of the amyloid beta-protein (Abeta), are hallmark neuropathological lesions in Alzheimer disease (AD) brain.
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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.
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Astrocyte pathology occurs in association with Alzheimer's disease (AD) and in brain ageing, but is poorly characterised.
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Researchers extracted soluble amyloid-beta protein oligomers directly from the cerebral cortex of subjects with Alzheimer's disease to study their impact.
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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.
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Apolipoprotein E is associated with age-related risk for Alzheimer's disease and plays critical roles in Abeta homeostasis.
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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.
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Autophagy is the principal cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress.
From across this tag
9 of the 1,611 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.
- APOE interacts with ACE2 inhibiting SARS-CoV-2 cellular entry and inflammation in COVID-19 patients
- ATG5 (autophagy related 5) in microglia controls hippocampal neurogenesis in Alzheimer disease
- Alzheimer amyloid protein precursor in the rat hippocampus: transport and processing through the perforant path
- Microarray analysis of hippocampal CA1 neurons implicates early endosomal dysfunction during Alzheimer's disease progression
- Electroacupuncture ameliorates beta-amyloid pathology and cognitive impairment in Alzheimer disease via a novel mechanism involving activation of TFEB (transcription factor EB)
- Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease
- Abeta toxicity in Alzheimer's disease: globular oligomers (ADDLs) as new vaccine and drug targets
- Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease
- Melatonin reverses the profibrillogenic activity of apolipoprotein E4 on the Alzheimer amyloid Abeta peptide