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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

1,365 studies carry this tag.

Date range

1982 to 2026

Top journals

  • Neurology 92
  • The Journal of biological chemistry 68
  • Proceedings of the National Academy of Sciences of the United States of America 47
  • Archives of neurology 43
  • JAMA neurology 36

375 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. Fine mapping of the chromosome 12 late-onset Alzheimer disease locus: potential genetic and phenotypic heterogeneity

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. American journal of human genetics 2000-03-01 Genetics

    Apolipoprotein E (APOE) is the only confirmed susceptibility gene for late-onset Alzheimer disease (AD).

  2. Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences 2000-02-29 Genetics

    Apolipoprotein E (apoE) alleles determine the age-adjusted relative risk (epsilon4 > epsilon3) for Alzheimer's disease (AD).

  3. Endogenous estrogen levels and Alzheimer's disease among postmenopausal women

    ✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurology 2000-02-01 Vascular contributions

    The results of this preliminary case-control study suggest that estradiol levels may decline significantly in women in whom AD develops.

  4. Lack of an association of estrogen receptor alpha gene polymorphisms and transcriptional activity with Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Archives of neurology 2000-02-01 Risk genes beyond APOE

    Long-term cognitive decline in postmenopausal women is associated with aging and Alzheimer disease (AD).

  5. High prevalence of pathogenic mutations in patients with early-onset dementia detected by sequence analyses of four different genes

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. American journal of human genetics 2000-01-01 Risk genes beyond APOE

    Clinical differential diagnosis of early-onset dementia (EOD) includes familial Alzheimer disease (FAD) and hereditary prion disease.

  6. Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature 1999-12-01 Disease mechanisms

  7. Purification and cloning of amyloid precursor protein β-secretase from human brain

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature 1999-12-01 Disease mechanisms

  8. Soluble pool of A? amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of Neurology 1999-12-01 Disease mechanisms

    Genetic evidence strongly supports the view that Abeta amyloid production is central to the cause of Alzheimer's disease.

  9. Cyclooxygenase-1 in human Alzheimer and control brain: quantitative analysis of expression by microglia and CA3 hippocampal neurons

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 1999-11-01 Inflammation and the immune system

    Epidemiological and clinical studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX) slow the progression and delay the onset of Alzheimer disease (AD).

  10. Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in equidae

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Equine veterinary journal 1999-11-01 Biomarkers

    In 3 mature female horses of varying breeds, episodes of colic and depression for 14 days preceded an encephalopathic disorder with maniacal behaviour, anxiety, profuse sweating and, in one case, terminal opisthotonus.

  11. β-Secretase Cleavage of Alzheimer's Amyloid Precursor Protein by the Transmembrane Aspartic Protease BACE

    ✓ Peer-reviewed alzhub usefulness score 64 out of 100. Science 1999-10-22 Disease mechanisms

    Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease.

  12. Evidence for an interaction between apolipoprotein E genotype, gender, and Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 61 out of 100. Alzheimer disease and associated disorders 1999-10-01 Genetics

    Carriers of the apolipoprotein E (APOE) epsilon4 allele show significantly higher risk of Alzheimer disease (AD).

  13. Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of neuropathology and experimental neurology 1999-09-01 Risk genes beyond APOE

    Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta).

  14. Oxidative damage and protection by antioxidants in the frontal cortex of Alzheimer's disease is related to the apolipoprotein E genotype

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Free radical biology & medicine 1999-09-01 Genetics

    A great number of epidemiological studies have demonstrated that the frequency of the epsilon4 allele of the apolipoprotein E gene (APOE) is markedly higher in sporadic and in familial late onset Alzheimer disease (AD).

  15. Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. American Journal Of Pathology 1999-09-01 Disease mechanisms

  16. Activation of neuronal caspase-3 by intracellular accumulation of wild-type Alzheimer amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 34 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1999-08-01 Risk genes beyond APOE

    Forced overexpression of wild-type Alzheimer amyloid precursor protein (APP) causes postmitotic neurons to degenerate.

  17. APOE-epsilon4 count predicts age when prevalence of AD increases, then declines: the Cache County Study

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 1999-07-01 Risk factors

    In participants with no epsilon4 alleles, the age-specific prevalence of AD reached a maximum and then declined after age 95.

  18. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Nature 1999-07-01 Risk genes beyond APOE

    Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD).

  19. The apolipoprotein E epsilon2 allele and the pathological features in cerebral amyloid angiopathy-related hemorrhage

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of neuropathology and experimental neurology 1999-07-01 Genetics

    Cerebral amyloid angiopathy (CAA) is associated with apolipoprotein E (APOE gene, apoE protein) polymorphism: current evidence suggests that the epsilon4 allele is a risk factor for the development of CAA and the epsilon2 allele predisposes to hemorrhage.

  20. A stop-codon mutation in the BRI gene associated with familial British dementia

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature 1999-06-01 Brain tissue and pathology

    Familial British dementia (FBD), previously designated familial cerebral amyloid angiopathy-British type, is an autosomal dominant disorder of undetermined origin characterized by progressive dementia, spasticity, and cerebellar ataxia, with onset at around the fifth decade of life.

  21. Crystal structure of the N-terminal, growth factor-like domain of Alzheimer amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 44 out of 100. Nature structural biology 1999-04-01 Risk genes beyond APOE

    Amyloid precursor protein (APP) plays a central role in Alzheimer disease.

  22. Differential effects of apolipoprotein E isoforms on metal-induced aggregation of A beta using physiological concentrations

    ✓ Peer-reviewed alzhub usefulness score 44 out of 100. Biochemistry 1999-04-01 Genetics

    The epsilon 4 allele of apolipoprotein E (APOE) has been found to be a risk factor for late-onset Alzheimer's disease (AD).

  23. Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5'-untranslated region sequences

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 1999-03-01 Risk genes beyond APOE

    The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD.

  24. Age of onset in Huntington disease: sex specific influence of apolipoprotein E genotype and normal CAG repeat length

    ✓ Peer-reviewed alzhub usefulness score 35 out of 100. Journal of medical genetics 1999-02-01 Genetics

    Age of onset (AO) of Huntington disease (HD) is known to be correlated with the length of an expanded CAG repeat in the HD gene.

  25. Endoplasmic reticulum and trans-Golgi network generate distinct populations of Alzheimer beta-amyloid peptides

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-01-01 Risk genes beyond APOE

    The excessive generation and accumulation of 40- and 42-aa beta-amyloid peptides (Abeta40/Abeta42) in selectively vulnerable brain regions is a major neuropathological feature of Alzheimer's disease.

  26. TNFalpha plus IFNgamma induce the production of Alzheimer beta-amyloid peptides and decrease the secretion of APPs

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1999-01-01 Risk genes beyond APOE

    The appearance of inflammatory markers associated with amyloid plaques indicates a state of chronic inflammation in Alzheimer's disease (AD).

  27. Alzheimer amyloid protein precursor in the rat hippocampus: transport and processing through the perforant path

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1998-12-01 Risk genes beyond APOE

    Amyloid deposition is a neuropathological hallmark of Alzheimer's disease.

  28. Caspase dependent DNA fragmentation might be associated with excitotoxicity in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neuropathology and experimental neurology 1998-11-01 Risk genes beyond APOE

    Recent studies have shown that deficient functioning of glutamate transporters (GTs) in Alzheimer disease (AD) might lead to neurodegeneration via excitotoxicity; however, the characteristics of cell death and pathways involved are not yet clear.

  29. Generation and regulation of beta-amyloid peptide variants by neurons

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neurochemistry 1998-11-01 Risk genes beyond APOE

    Studies of processing of the Alzheimer beta-amyloid precursor protein (betaAPP) have been performed to date mostly in continuous cell lines and indicate the existence of two principal metabolic pathways: the "beta-secretase" pathway, which generates beta-amyloid (A beta(1-40/42); approximately 4 kDa), and the "alpha-secretase" pathway, which generates a smaller fragment, the "p3" peptide (A beta(17-40/42); approximately 3 kDa).

  30. Microglial activation induced by factor(s) contained in sera from Alzheimer-related ApoE genotypes

    ✓ Peer-reviewed alzhub usefulness score 35 out of 100. Journal of neuroscience research 1998-11-01 Down syndrome and Alzheimer's

    The risk of developing AD definitely increases with (a) age, (b) head injuries, (c) family history of AD or Down syndrome, (d) sex (higher prevalence of AD in women), (e) vascular disease, (f) exposure to environmental toxins, (g) infectious processes, or (h) changes in immune function, and recent advances in molecular genetics have suggested that genetic predisposition (i) can be considered one of the most important risk factors in the development of AD.

  31. Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The American journal of pathology 1998-10-01 Genetics

    Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease.

  32. HIV-infected subjects with the E4 allele for APOE have excess dementia and peripheral neuropathy

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature medicine 1998-10-01 Genetics

    HIV produces a chronic viral infection of the central nervous system that elicits chronic glial activation and overexpression of glial cytokines that are also implicated in Alzheimer disease (AD) pathogenesis.

  33. Alpha-2 macroglobulin is genetically associated with Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature genetics 1998-08-01 Genetics

    Alpha-2-macroglobulin (alpha-2M; encoded by the gene A2M) is a serum pan-protease inhibitor that has been implicated in Alzheimer disease (AD) based on its ability to mediate the clearance and degradation of A beta, the major component of beta-amyloid deposits.

  34. Evidence for an Alzheimer disease susceptibility locus on chromosome 12 and for further locus heterogeneity

    ✓ Peer-reviewed alzhub usefulness score 60 out of 100. JAMA 1998-08-01 Genetics

    Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families.

  35. Apolipoprotein E genotype and deposits of Abeta40 and Abeta42 in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Archives of neurology 1998-07-01 Risk genes beyond APOE

    Previous data from familial AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein suggest that the long form of Abeta peptide, Abeta42, is selectively increased in these circumstances.

  36. Microglial activation in Alzheimer disease: Association with APOE genotype

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain pathology (Zurich, Switzerland) 1998-07-01 Genetics

    Microglial cells are considered to play an important role in the pathogenesis of Alzheimer disease.

  37. Risk estimates of dementia by apolipoprotein E genotypes from a population-based incidence study: the Rotterdam Study

    ✓ Peer-reviewed alzhub usefulness score 69 out of 100. Archives of neurology 1998-07-01 Genetics

    The APOE genotype is an important determinant of the risk of dementia.

  38. Distribution of reducible 4-hydroxynonenal adduct immunoreactivity in Alzheimer disease is associated with APOE genotype

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neuropathology and experimental neurology 1998-05-01 Genetics

    Two major risk factors for late-onset familial and sporadic Alzheimer disease (AD), a leading cause of dementia worldwide, are increasing age and inheritance of the epsilon4 allele of the apolipoprotein E gene (APOE4).

  39. Degeneration in vivo of rat hippocampal neurons by wild-type Alzheimer amyloid precursor protein overexpressed by adenovirus-mediated gene transfer

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1998-04-01 Risk genes beyond APOE

    In an attempt to elucidate the pathological implications of intracellular accumulation of the amyloid precursor protein (APP) in postmitotic neurons in vivo, we transferred APP695 cDNA into rat hippocampal neurons by using a replication-defective adenovirus vector.

  40. Phosphatidylinositol and inositol involvement in Alzheimer amyloid-beta fibril growth and arrest

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of molecular biology 1998-04-01 Risk genes beyond APOE

    A key pathological feature of Alzheimer's disease is the formation and accumulation of amyloid fibres.

  41. Hippocampal atrophy and apolipoprotein E genotype are independently associated with Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Annals of neurology 1998-03-01 Hippocampus size on brain scans

    A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD).

  42. The APOE-epsilon4 allele and the risk of Alzheimer disease among African Americans, whites, and Hispanics

    ✓ Peer-reviewed alzhub usefulness score 70 out of 100. JAMA 1998-03-01 Genetics

    The presence of an APOE-epsilon4 allele is a determinant of AD risk in whites, but African Americans and Hispanics have an increased frequency of AD regardless of their APOE genotype.

  43. Utility of the apolipoprotein E genotype in the diagnosis of Alzheimer's disease. Alzheimer's Disease Centers Consortium on Apolipoprotein E and Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 61 out of 100. The New England journal of medicine 1998-02-01 Getting a diagnosis

    APOE genotyping does not provide sufficient sensitivity or specificity to be used alone as a diagnostic test for Alzheimer's disease, but when used in combination with clinical criteria, it improves the specificity of the diagnosis.

  44. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 1998-01-01 Risk genes beyond APOE

    Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes.

  45. Mutant genes in familial Alzheimer's disease and transgenic models

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Annual review of neuroscience 1998-01-01 Brain tissue and pathology

    The most common cause of dementia occurring in mid- to late-life is Alzheimer's disease (AD).

  46. Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature Genetics 1997-11-01 Genetics

  47. Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-11-01 Risk genes beyond APOE

    Mutations in the amyloid precursor protein (APP) gene cause early-onset familial Alzheimer disease (AD) by affecting the formation of the amyloid beta (A beta) peptide, the major constituent of AD plaques.

  48. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 1997-10-01 Risk genes beyond APOE

    Missense mutations in two related genes, termed presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees.

  49. Complete genomic screen in late-onset familial Alzheimer disease. Evidence for a new locus on chromosome 12

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. JAMA 1997-10-01 Genetics

    Fifteen chromosomal regions warranted initial follow-up.

  50. Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes epsilon2/epsilon4 (OR=2.6, 95% CI=1.6-4.0), epsilon3/epsilon4 (OR=3.2, 95% CI=2.8-3.8), and epsilon4/epsilon4 (OR=14.9, 95% CI= 10.8-20.6); whereas, the ORs were decreased for people with genotypes epsilon2/epsilon2 (OR=0.6, 95% CI=0.2-2.0) and epsilon2/epsilon3 (OR=0.6, 95% CI=0.5-0.8).

From across this tag

10 of the 1,363 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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