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Home › Research › Topics › apoe

apoe

1,350 studies tagged apoe, dated 1982-09-01 to 2026-10-18. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Evidence for Reduced Somatic T-Cell Receptor Sequence Diversity Profiles Among Midwestern Amish in an Aging Cohort Study 2026-10-18
  2. Gantenerumab reduces brain amyloid-β proteoforms: Biochemical evaluation in dominantly inherited Alzheimer disease 2026-09-29
  3. Genetic Insights Into Protective Effects of GLP-1 Receptor Agonists on Stroke and Alzheimer Disease Across Ancestries 2026-09-25

Studies

1,350 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.

  1. LR11/SorLA expression is reduced in sporadic Alzheimer disease but not in familial Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neuropathology and experimental neurology 2006-09-01 Genetics

    LR11 is an ApoE receptor that is enriched in the brain.

  2. APP duplication is sufficient to cause early onset Alzheimer's dementia with cerebral amyloid angiopathy

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Brain : a journal of neurology 2006-08-18 Brain tissue and pathology

    We assessed the impact of amyloid precursor protein (APP) gene locus duplications in early onset Alzheimer's disease in a Dutch population-based sample.

  3. Shorter telomeres are associated with mortality in those with APOE epsilon4 and dementia

    ✓ Peer-reviewed alzhub usefulness score 60 out of 100. Annals of neurology 2006-08-01 Disparities

    We hypothesized that telomere length might thus relate to increased risk for dementia and mortality.

  4. Age and apolipoprotein E*4 allele effects on cerebrospinal fluid beta-amyloid 42 in adults with normal cognition

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Archives of neurology 2006-07-01 Genetics

    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.

  5. Mean age-of-onset of familial alzheimer disease caused by presenilin mutations correlates with both increased Abeta42 and decreased Abeta40

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Human mutation 2006-07-01 Risk genes beyond APOE

    The varied ways in which mutations in presenilins (PSEN1 and PSEN2) affect amyloid b precursor protein (APP) processing in causing early-onset familial Alzheimer disease (FAD) are complex and not yet properly understood.

  6. Increased proliferation reflects glial and vascular-associated changes, but not neurogenesis in the presenile Alzheimer hippocampus

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurobiology of disease 2006-06-30 Biomarkers

    Adult proliferation and hippocampal neurogenesis are stimulated by injury.

  7. Human amyloid-beta synthesis and clearance rates as measured in cerebrospinal fluid in vivo

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 2006-06-25 Risk genes beyond APOE

    Certain disease states are characterized by disturbances in production, accumulation or clearance of protein.

  8. Do axonal defects in tau and amyloid precursor protein transgenic animals model axonopathy in Alzheimer's disease?

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of neurochemistry 2006-06-19 Risk genes beyond APOE

    The subcellular localization of organelles, mRNAs and proteins is particularly challenging in neurons.

  9. Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of biological chemistry 2006-06-02 Risk genes beyond APOE

    Nicotinamide adenine dinucleotide (NAD)+-dependent sirtuins have been identified to be key regulators in the lifespan extending effects of calorie restriction (CR) in a number of species.

  10. High levels of Alzheimer beta-amyloid precursor protein (APP) in children with severely autistic behavior and aggression

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of child neurology 2006-06-01 Risk genes beyond APOE

    Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication.

  11. Decreased RNA, and increased RNA oxidation, in ribosomes from early Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neurochemical research 2006-05-23 Mild cognitive impairment

    All cells rely on efficient protein synthesis in order to maintain cellular homeostasis.

  12. Coronary artery disease is associated with Alzheimer disease neuropathology in APOE4 carriers

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurology 2006-05-01 Genetics

    The degree of coronary artery disease is independently associated with the cardinal neuropathological lesions of Alzheimer disease.

  13. The influence of Alzheimer disease family history and apolipoprotein E epsilon4 on mesial temporal lobe activation

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2006-05-01 Genetics

    First-degree family history of sporadic Alzheimer disease (AD) and the apolipoprotein E epsilon4 (APOE4) are risk factors for developing AD.

  14. Degradation of the Alzheimer disease amyloid beta-peptide by metal-dependent up-regulation of metalloprotease activity

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2006-04-28 Risk genes beyond APOE

    Biometals play an important role in Alzheimer disease, and recent reports have described the development of potential therapeutic agents based on modulation of metal bioavailability.

  15. Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2006-04-25 Risk genes beyond APOE

    The deficits characteristic of Alzheimer's disease (AD) are believed to result, at least in part, from the neurotoxic effects of beta-amyloid peptides, a set of 39-43 amino acid fragments derived proteolytically from beta-amyloid precursor protein (APP).

  16. Promoter mutations that increase amyloid precursor-protein expression are associated with Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. American journal of human genetics 2006-04-10 Down syndrome and Alzheimer's

    Genetic variations in promoter sequences that alter gene expression play a prominent role in increasing susceptibility to complex diseases.

  17. Altered brain white matter integrity in healthy carriers of the APOE epsilon4 allele: a risk for AD?

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neurology 2006-04-01 Genetics

    Although the mechanism underlying vulnerability of white matter tracts in APOE epsilon4 carriers is still unknown, these findings suggest that increased genetic risk for developing Alzheimer disease is associated with changes in microscopic white matter integrity well before the onset of dementia.

  18. Mechanisms behind the neuroprotective actions of cholinesterase inhibitors in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Alzheimer disease and associated disorders 2006-04-01 Risk genes beyond APOE

    Inhibitors of the enzyme acetylcholinesterase (AChE) are presently used as long-term symptomatic treatments for patients with Alzheimer disease (AD), as they enhance central levels of synaptic acetylcholine.

  19. Interleukin-1 mediates Alzheimer and Lewy body pathologies

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of neuroinflammation 2006-03-16 Risk genes beyond APOE

    Clinical and neuropathological overlap between Alzheimer's (AD) and Parkinson's disease (PD) is now well recognized.

  20. Poor sleep is associated with higher plasma proinflammatory cytokine interleukin-6 and procoagulant marker fibrin D-dimer in older caregivers of people with Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of the American Geriatrics Society 2006-03-01 Prevention and risk

    These effects were most pronounced in caregivers of subjects with Alzheimer's disease.

  21. Redox proteomics identification of oxidatively modified hippocampal proteins in mild cognitive impairment: insights into the development of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neurobiology of disease 2006-02-08 Mild cognitive impairment

    Mild cognitive impairment (MCI) is generally referred to the transitional zone between normal cognitive function and early dementia or clinically probable Alzheimer's disease (AD).

  22. Alzheimer precursor protein interaction with the Nogo-66 receptor reduces amyloid-beta plaque deposition

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2006-02-01 Risk genes beyond APOE

    Pathophysiologic hypotheses for Alzheimer's disease (AD) are centered on the role of the amyloid plaque Abeta peptide and the mechanism of its derivation from the amyloid precursor protein (APP).

  23. Bone Marrow-Derived Microglia Play a Critical Role in Restricting Senile Plaque Formation in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neuron 2006-02-01 Inflammation and the immune system

  24. Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2006-02-01 Risk genes beyond APOE

    Locus ceruleus (LC) degeneration and loss of cortical noradrenergic innervation occur early in Alzheimer's disease (AD).

  25. The neuropeptide PACAP promotes the alpha-secretase pathway for processing the Alzheimer amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2006-01-09 Risk genes beyond APOE

    The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has neurotrophic as well as anti-apoptotic properties and is involved in learning and memory processes.

  26. Amyloidogenic processing of beta-amyloid precursor protein in intracellular compartments

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurology 2006-01-01 Risk genes beyond APOE

    Trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations in the past two decades, since the identification of Abeta as the principal component of brain senile plaques and the cloning of APP cDNA.

  27. Apolipoprotein E genotype and age-related myelin breakdown in healthy individuals: implications for cognitive decline and dementia

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of general psychiatry 2006-01-01 Genetics

    In later-myelinating regions, the severity and rate of myelin breakdown in healthy older individuals are associated with APOE status and support the hypothesis that this process may contribute to age at onset of AD.

  28. Cholesterol, APOE genotype, and Alzheimer disease: an epidemiologic study of Nigerian Yoruba

    ✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01 Genetics

    There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans.

  29. Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy

    ✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01 Genetics

    If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly.

  30. The cerebral beta-amyloid angiopathies: hereditary and sporadic

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Brain pathology (Zurich, Switzerland) 2006-01-01 Risk genes beyond APOE

    We review the clinical, radiologic, and neuropathologic features of the hereditary and sporadic forms of cerebral amyloid angiopathy (CAA) associated with vascular deposition of the beta-amyloid peptide.

  31. APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature genetics 2005-12-20 Brain tissue and pathology

    We report duplication of the APP locus on chromosome 21 in five families with autosomal dominant early-onset Alzheimer disease (ADEOAD) and cerebral amyloid angiopathy (CAA).

  32. Activation of Toll-like receptor 2 on microglia promotes cell uptake of Alzheimer disease-associated amyloid beta peptide

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2005-12-09 Inflammation and the immune system

    The human G-protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homologue mFPR2 mediate the chemotactic activity of a variety of polypeptides associated with inflammation and bacterial infection, including the 42-amino acid form of amyloid beta peptide (Abeta42), a pathogenic factor in Alzheimer disease.

  33. APOE alleles predict the rate of cognitive decline in Alzheimer disease: a nonlinear model

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology 2005-12-01 Genetics

    APOE genotype strongly predicts the rate of cognitive decline in Alzheimer disease.

  34. Novel presenilin 1 mutation (S170F) causing Alzheimer disease with Lewy bodies in the third decade of life

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Archives of neurology 2005-12-01 Risk genes beyond APOE

    Cases of early-onset Alzheimer disease (AD) with an autosomal dominant inheritance pattern (familial AD [FAD]) are rare but have greatly advanced our understanding of the molecular pathogenesis of AD.

  35. Amyloid precursor protein-mediated free radicals and oxidative damage: implications for the development and progression of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neurochemistry 2005-11-23 Brain tissue and pathology

    Alzheimer's disease (AD) is a late-onset dementia that is characterized by the loss of memory and an impairment of multiple cognitive functions.

  36. Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. PLoS medicine 2005-11-15 Risk genes beyond APOE

    The proteases (secretases) that cleave amyloid-beta (Abeta) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease.

  37. Circulating levels of soluble receptor for advanced glycation end products in Alzheimer disease and vascular dementia

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Archives of neurology 2005-11-01 Disease mechanisms

    Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls.

  38. P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of clinical investigation 2005-10-20 Risk genes beyond APOE

    Accumulation of amyloid-beta (Abeta) within extracellular spaces of the brain is a hallmark of Alzheimer disease (AD).

  39. Deletion of Abca1 increases Abeta deposition in the PDAPP transgenic mouse model of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 2005-10-05 Genetics

    Apolipoprotein E (apoE) genotype has a major influence on the risk for Alzheimer disease (AD).

  40. Lack of ABCA1 considerably decreases brain ApoE level and increases amyloid deposition in APP23 mice

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2005-10-05 Genetics

    ABCA1 (ATP-binding cassette transporter A1) is a major regulator of cholesterol efflux and high density lipoprotein (HDL) metabolism.

  41. The absence of ABCA1 decreases soluble ApoE levels but does not diminish amyloid deposition in two murine models of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2005-10-05 Genetics

    ABCA1, a cholesterol transporter expressed in the brain, has been shown recently to be required to maintain normal apoE levels and lipidation in the central nervous system.

  42. The role of apoptotic pathways in Alzheimer's disease neurodegeneration and cell death

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Current Alzheimer research 2005-10-01 Disease mechanisms

    Neuronal loss is associated with Alzheimer's disease (AD).

  43. Amyloid beta-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2005-09-09 Risk genes beyond APOE

    Human genetic data have associated angiotensin-converting enzyme (ACE) with Alzheimer disease (AD), and purified ACE has been reported to cleave synthetic amyloid beta-protein (Abeta) in vitro.

  44. Dynamic complexity of the microglial activation response in transgenic models of amyloid deposition: implications for Alzheimer therapeutics

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of neuropathology and experimental neurology 2005-09-01 Risk genes beyond APOE

    The presence of activated microglia in postmortem Alzheimer disease specimens is used to support the argument that inflammation contributes to Alzheimer pathogenesis.

  45. Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature neuroscience 2005-08-28 Risk genes beyond APOE

    In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with neurodegeneration and accumulation of amyloid precursor protein (APP) products.

  46. Modulation of apolipoprotein E structure by domain interaction: differences in lipid-bound and lipid-free forms

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2005-08-01 Genetics

    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.

  47. BRI2 interacts with amyloid precursor protein (APP) and regulates amyloid beta (Abeta) production

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2005-07-18 Risk genes beyond APOE

    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.

  48. Regulation of NMDA receptor trafficking by amyloid-beta

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature neuroscience 2005-07-17 Disease mechanisms

    Amyloid-beta peptide is elevated in the brains of patients with Alzheimer disease and is believed to be causative in the disease process.

  49. Beta-amyloid-induced dynamin 1 depletion in hippocampal neurons. A potential mechanism for early cognitive decline in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2005-07-07 Disease mechanisms

    Synaptic dysfunction is one of the earliest events in the pathogenesis of Alzheimer disease (AD).

  50. Increased levels of 4-hydroxynonenal and acrolein, neurotoxic markers of lipid peroxidation, in the brain in Mild Cognitive Impairment and early Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurobiology of aging 2005-07-01 Mild cognitive impairment

    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.

From across this tag

10 of the 1,348 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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