ArticleNeurobiology of aging2014
A 2-process model for neuropathology of Alzheimer's disease.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Smoking and increased Alzheimer's disease risk: a review of potential mechanisms.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014Pooled it
- Global and regional amyloid-β in explaining APOE-ε4 and sex associations with medial temporal tau: a neuropathology study.Acta neuropathologica · 2026Article
- A critical appraisal of the link between apolipoprotein E and Tau.Current opinion in neurology · 2026Review
- Circulating C-reactive protein influences polygenic risk of inflammatory genes expressed in brain endothelia for Alzheimer's disease.Neurobiology of disease · 2026Article
- Patterns of tau, amyloid and synuclein pathology in ageing, Alzheimer's disease and synucleinopathies.Brain : a journal of neurology · 2025Article
- Are current etiological theories of Alzheimer's disease falsifiable? An epistemological assessment.Frontiers in aging neuroscience · 2025Article
- Multifaceted roles of APOE in Alzheimer disease.Nature reviews. Neurology · 2024Review
- Age-, sex-, and pathology-related variability in brain structure and cognition.Translational psychiatry · 2023Article
- Visual reading for [Frontiers in neuroscience · 2023Article
- Genome-wide association study and functional validation implicates JADE1 in tauopathy.Acta neuropathologica · 2022Article
- Longitudinal CSF Alzheimer's disease biomarker changes from middle age to late adulthood.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- Differential associations of APOE-ε2 and APOE-ε4 alleles with PET-measured amyloid-β and tau deposition in older individuals without dementia.European journal of nuclear medicine and molecular imaging · 2021Article
- Association of Cigarette Smoking With Cerebrospinal Fluid Biomarkers of Neurodegeneration, Neuroinflammation, and Oxidation.JAMA network open · 2020Article
- Positron Emission Tomography Imaging With [18F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes.JAMA neurology · 2020Article
- Comparison of regional flortaucipir PET with quantitative tau immunohistochemistry in three subjects with Alzheimer's disease pathology: a clinicopathological study.EJNMMI research · 2020Article
- Genetic risk for Alzheimer's disease influences neuropathology via multiple biological pathways.Brain communications · 2020Article
- A multicentre longitudinal study of flortaucipir (18F) in normal ageing, mild cognitive impairment and Alzheimer's disease dementia.Brain : a journal of neurology · 2019Article
- Late-life blood pressure association with cerebrovascular and Alzheimer disease pathology.Neurology · 2018Article
- Combined neuropathological pathways account for age-related risk of dementia.Annals of neurology · 2018Article
- Early Alzheimer-type lesions in cognitively normal subjects.Neurobiology of aging · 2018Article
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5 authors.
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Abstract
This study examined relations among neuritic and diffuse plaques, neurofibrillary tangles, age, and apolipoprotein E (APOE) in 2 large samples of neuropathology cases, the Religious Orders Study and the Memory and Aging Project. Cognitive status ranged from normal to demented and AD neuropathology ranged from none to severe. Confirmatory factor analysis identified a best-fitting 4-factor solution to describe interrelationships among plaques and tangles: a global neuritic plaque factor; a global diffuse plaque factor; a factor defined by medial temporal neurofibrillary tangles; and a neocortical tangle factor. Results supported a hypothesis that neuritic plaques mediate the association of age and APOE with neocortical tangles, and similarly mediate the effect of APOE on medial temporal tangles. However, medial temporal tangles were related to age independent of neuritic plaques. These results support a primary amyloid-based AD process that accounts for neocortical tangles and makes the largest contribution to medial temporal tangles. A second, age-related but non-amyloid process likely contributes to medial temporal lobe tangles.
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