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Home › Research › Topics › apolipoprotein

apolipoprotein

1,613 studies tagged apolipoprotein, dated 1982-09-01 to 2026-10-27. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. ApoE4 and Psychosis in Neurodegenerative and Non-Neurodegenerative Disease: A Scoping Review 2026-10-27
  2. Multimodal mediators connecting APOE4 to dementia 2026-10-21
  3. Reproductive Aging, FSH, and Apolipoprotein Biology in Alzheimer’s Disease 2026-10-19

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.

  1. Cerebrospinal fluid APOE levels: an endophenotype for genetic studies for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Human molecular genetics 2012-07-20 Genetics

    The apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer's disease (AD).

  2. Novel late-onset Alzheimer disease loci variants associate with brain gene expression

    ✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2012-06-20 Genetics

    CLU and MS4A4A eSNPs may at least partly explain the LOAD risk association at these loci.

  3. Identification of Alzheimer disease-associated variants in genes that regulate retromer function

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurobiology of aging 2012-06-05 Risk genes beyond APOE

    The proteolytic processing of amyloid precursor protein (APP) to generate the neurotoxic amyloid β (Aβ) peptide is central to the pathogenesis of Alzheimer disease (AD).

  4. Apolipoprotein E ε4 and age effects on florbetapir positron emission tomography in healthy aging and Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurobiology of aging 2012-05-24 Brain scans and imaging

    Cerebral amyloid deposition is associated with APOE4 carrier status in older healthy control subjects and symptomatic AD patients, and increases with age in older cognitively normal individuals.

  5. Cigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. PloS one 2012-05-11 Risk genes beyond APOE

    Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD).

  6. Exercise is more effective than diet control in preventing high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2012-05-04 Risk genes beyond APOE

    Accumulating evidence suggests that some dietary patterns, specifically high fat diet (HFD), increase the risk of developing sporadic Alzheimer disease (AD).

  7. Serum antibodies to periodontal pathogens are a risk factor for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2012-05-01 Mild cognitive impairment

    This study provides initial data that demonstrate elevated antibodies to periodontal disease bacteria in subjects years before cognitive impairment and suggests that periodontal disease could potentially contribute to the risk of AD onset/progression.

  8. Genotype patterns at PICALM, CR1, BIN1, CLU, and APOE genes are associated with episodic memory

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2012-04-25 Genetics

    MLGPs provide an alternative analytical approach to predict an individual's genetic risk for episodic memory performance, a surrogate indicator of LOAD.

  9. Generation of Alzheimer disease-associated amyloid β42/43 peptide by γ-secretase can be inhibited directly by modulation of membrane thickness

    ✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2012-04-24 Risk genes beyond APOE

    Pathogenic generation of amyloid β-peptide (Aβ) by sequential cleavage of β-amyloid precursor protein (APP) by β- and γ-secretases is widely believed to causally underlie Alzheimer disease (AD). β-Secretase initially cleaves APP thereby generating a membrane-bound APP C-terminal fragment, from which γ-secretase subsequently liberates 37-43-amino acid long Aβ species.

  10. The mechanism of γ-Secretase dysfunction in familial Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. The EMBO journal 2012-04-13 Risk genes beyond APOE

    The mechanisms by which mutations in the presenilins (PSEN) or the amyloid precursor protein (APP) genes cause familial Alzheimer disease (FAD) are controversial.

  11. Glutathione S-transferase omega genes in Alzheimer and Parkinson disease risk, age-at-diagnosis and brain gene expression: an association study with mechanistic implications

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Molecular neurodegeneration 2012-04-11 Genetics

    These results suggest that GSTO locus variants may lower brain GSTO2 levels and consequently confer AD risk in older age.

  12. High frequency of potentially pathogenic SORL1 mutations in autosomal dominant early-onset Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular psychiatry 2012-04-03 Risk genes beyond APOE

    Performing exome sequencing in 14 autosomal dominant early-onset Alzheimer disease (ADEOAD) index cases without mutation on known genes (amyloid precursor protein (APP), presenilin1 (PSEN1) and presenilin2 (PSEN2)), we found that in five patients, the SORL1 gene harbored unknown nonsense (n=1) or missense (n=4) mutations.

  13. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. Cell 2012-04-01 Risk genes beyond APOE

    Alzheimer's disease (AD) results in cognitive decline and altered network activity, but the mechanisms are unknown.

  14. Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Cold Spring Harbor perspectives in medicine 2012-03-01 Genetics

    Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective.

  15. Resting metabolic connectivity in prodromal Alzheimer's disease. A European Alzheimer Disease Consortium (EADC) project

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurobiology of aging 2012-02-23 Brain scans and imaging

    We explored resting-state metabolic connectivity in prodromal Alzheimer's disease (pAD) patients and in healthy controls (CTR), through a voxel-wise interregional correlation analysis of 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) by means of statistical parametric mapping.

  16. ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2012-02-09 Genetics

    Alzheimer's disease (AD) is associated with impaired clearance of β-amyloid (Aβ) from the brain, a process normally facilitated by apolipoprotein E (apoE).

  17. Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Antioxidants & redox signaling 2012-02-07 Mild cognitive impairment

    Alzheimer's disease (AD) is the most common cause of dementia and a progressive neurodegeneration that appears to result from multiple pathogenic mechanisms (including protein misfolding/aggregation, involved in both amyloid β-dependent senile plaques and tau-dependent neurofibrillary tangles), metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction, neuroinflammation, and oxidative stress.

  18. Accelerated cortical atrophy in cognitively normal elderly with high β-amyloid deposition

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurology 2012-02-01 Brain scans and imaging

    Our findings show that the presence of Aβ in the brain, known to occur in about one-third of asymptomatic elderly individuals, is actually a pathologic state associated with accelerated atrophy.

  19. β-Amyloid burden in healthy aging: regional distribution and cognitive consequences

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurology 2012-02-01 Genetics

    Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status.

  20. Rare variants in APP, PSEN1 and PSEN2 increase risk for AD in late-onset Alzheimer's disease families

    ✓ Peer-reviewed alzhub usefulness score 59 out of 100. PloS one 2012-02-01 Brain tissue and pathology

    Pathogenic mutations in APP, PSEN1, PSEN2, MAPT and GRN have previously been linked to familial early onset forms of dementia.

  21. CCL2 is associated with a faster rate of cognitive decline during early stages of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. PloS one 2012-01-30 Mild cognitive impairment

    Chemokine (C-C motif) receptor 2 (CCR2)-signaling can mediate accumulation of microglia at sites affected by neuroinflammation.

  22. Both common variations and rare non-synonymous substitutions and small insertion/deletions in CLU are associated with increased Alzheimer risk

    ✓ Peer-reviewed alzhub usefulness score 68 out of 100. Molecular neurodegeneration 2012-01-16 Genetics

    We identified a new genetic risk association of AD with rare coding CLU variations that is independent of the 5' common association signal identified in the GWA studies.

  23. APOE genotype alters glial activation and loss of synaptic markers in mice

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Glia 2012-01-06 Genetics

    The ε4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and affects clinical outcomes of chronic and acute brain damages.

  24. Contributions of brain insulin resistance and deficiency in amyloid-related neurodegeneration in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Drugs 2012-01-01 Prevention and risk

    Growing evidence supports the concept that AD is fundamentally a metabolic disease that results in progressive impairment in the brain's capacity to utilize glucose and respond to insulin and insulin-like growth factor (IGF) stimulation.

  25. The French series of autosomal dominant early onset Alzheimer's disease cases: mutation spectrum and cerebrospinal fluid biomarkers

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of Alzheimer's disease : JAD 2012-01-01 Risk genes beyond APOE

    We describe 56 novel autosomal dominant early-onset Alzheimer disease (ADEOAD) families with PSEN1, PSEN2, and AβPP mutations or duplications, raising the total of families with mutations on known genes to 111 (74 PSEN1, 8 PSEN2, 16 AβPP, and 13 AβPP duplications) in the French series.

  26. Hypoxia due to cardiac arrest induces a time-dependent increase in serum amyloid β levels in humans

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. PloS one 2011-12-14 Risk genes beyond APOE

    Amyloid β (Aβ) peptides are proteolytic products from amyloid precursor protein (APP) and are thought to play a role in Alzheimer disease (AD) pathogenesis.

  27. The association between a polygenic Alzheimer score and cortical thickness in clinically normal subjects

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Cerebral cortex (New York, N.Y. : 1991) 2011-12-13 Genetics

    Late-onset Alzheimer's disease (AD) is 50-70% heritable with complex genetic underpinnings.

  28. The miR-124 regulates the expression of BACE1/β-secretase correlated with cell death in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Toxicology letters 2011-12-08 Risk genes beyond APOE

    The role of miR-124 on the expression of β-site APP cleaving enzyme 1 (BACE1), an important cleavager of amyloid precursor protein that plays a pivotal role in the β-amyloid production, was studied in this paper using cellular models for Alzheimer' disease (AD) of cultured PC12 cell lines and primary cultured hippocampal neurons.

  29. Amyloid precursor protein revisited: neuron-specific expression and highly stable nature of soluble derivatives

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2011-12-05 Risk genes beyond APOE

    APP processing and amyloid-β production play a central role in Alzheimer disease pathogenesis.

  30. Apolipoprotein E promotes β-amyloid trafficking and degradation by modulating microglial cholesterol levels

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2011-11-30 Genetics

    Allelic variation in the apolipoprotein E (APOE) gene is the major risk factor of sporadic Alzheimer disease.

  31. Amyloid β: linking synaptic plasticity failure to memory disruption in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2011-11-28 Disease mechanisms

    Mounting evidence suggests that amyloid beta-induced impairments in synaptic plasticity that is accompanied by cognitive decline and dementia represent key pathogenic steps of Alzheimer's disease.

  32. The role of metallobiology and amyloid-β peptides in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neurochemistry 2011-11-28 Risk genes beyond APOE

    The biggest risk factor for Alzheimer's disease is the process of ageing, but the mechanisms that lead to the manifestation of the disease remain to be elucidated.

  33. Glutamatergic alterations and mitochondrial impairment in a murine model of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of aging 2011-10-27 Biomarkers

    Deficits in glutamate neurotransmission and mitochondrial functions were detected in the frontal cortex (FC) and hippopcampus (HIPP) of aged 3×Tg-Alzheimer's disease (AD) mice, compared with their wild type littermates (non-Tg).

  34. Alzheimer-specific variants in the 3'UTR of Amyloid precursor protein affect microRNA function

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2011-10-07 Risk genes beyond APOE

    APP expression misregulation can cause genetic Alzheimer's disease (AD).

  35. Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Annals of neurology 2011-10-01 Lewy body dementia

    The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of neurodegenerative disorders.

  36. Functions of the APP gene family in the nervous system: insights from mouse models

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Experimental brain research 2011-09-20 Risk genes beyond APOE

    The amyloid precursor protein (APP) plays a key role in the pathogenesis of Alzheimer's disease (AD), as proteolytical cleavage of APP gives rise to the β-amyloid peptide which is deposited in the brains of Alzheimer patients.

  37. Autosomal recessive causes likely in early-onset Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Archives of neurology 2011-09-12 Brain tissue and pathology

    A liability threshold model of disease was used to estimate heritability of EOAD and late-onset Alzheimer disease (AD) using concordance for AD among parent-offspring pairs.

  38. The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurobiology of learning and memory 2011-09-06 Getting a diagnosis

    Alzheimer's disease (AD) is the 3rd most costly disease and the leading cause of dementia.

  39. Association of Alzheimer disease pathology with abnormal lipid metabolism: the Hisayama Study

    ✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurology 2011-09-01 Genetics

    The results of this study suggest that dyslipidemia increases the risk of plaque-type pathology.

  40. Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia

    ✓ Peer-reviewed alzhub usefulness score 62 out of 100. Nature 2011-08-21 Lewy body dementia

    Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neuron degeneration in the brain and spinal cord.

  41. Association and expression analyses with single-nucleotide polymorphisms in TOMM40 in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2011-08-01 Genetics

    Although we did not replicate the earlier association between the APOE 3-TOMM40 haplotypes and age at onset, we observed that the polyT polymorphism is associated with risk of LOAD in APOE 33 homozygotes in a large case-control series but in the opposite direction as in the previous study.

  42. Directed conversion of Alzheimer's disease patient skin fibroblasts into functional neurons

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Cell 2011-08-01 Risk genes beyond APOE

    Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics.

  43. Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neuroreport 2011-08-01 Risk genes beyond APOE

    Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of β-amyloid precursor protein (βAPP), Aβ42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology.

  44. Reactive glia not only associates with plaques but also parallels tangles in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. The American journal of pathology 2011-07-21 Caregiving

    Senile plaques are a prominent pathological feature of Alzheimer's disease (AD), but little is understood about the association of glial cells with plaques or about the dynamics of glial responses through the disease course.

  45. The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Cell adhesion & migration 2011-07-01 Risk genes beyond APOE

    The amyloid-beta (Aβ) peptide is the derivative of amyloid precursor protein (APP) generated through sequential proteolytic processing by β- and γ-secretases.

  46. Human apoE Isoforms Differentially Regulate Brain Amyloid-β Peptide Clearance

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. Science Translational Medicine 2011-06-29 Genetics

    The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset, sporadic Alzheimer's disease (AD).

  47. Microarray analysis of the astrocyte transcriptome in the aging brain: relationship to Alzheimer's pathology and APOE genotype

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurobiology of aging 2011-06-25 Biomarkers

    Astrocytes contribute to a variety of functions in the brain, including homeostasis, synapse formation, plasticity, and metabolism.

  48. Precuneus amyloid burden is associated with reduced cholinergic activity in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurology 2011-06-22 Genetics

    Despite accumulating amyloid burden, cholinergic enzyme activity is stable in the precuneus during prodromal AD.

  49. Face-name associative memory performance is related to amyloid burden in normal elderly

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuropsychologia 2011-06-12 Caregiving

    Cerebral amyloid beta (Aβ) deposition occurs in a substantial fraction of cognitively normal (CN) older individuals.

  50. Deficient brain insulin signalling pathway in Alzheimer's disease and diabetes

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of pathology 2011-05-19 Risk factors

    Brain glucose metabolism is impaired in Alzheimer's disease (AD), the most common form of dementia.

From across this tag

10 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 10. The same 10 appear here every time.

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