ArticleJournal of Alzheimer's disease : JAD2018
Aβ42/Aβ40 Ratios of Presenilin 1 Mutations Correlate with Clinical Onset of Alzheimer's Disease.
Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases.MedComm · 2026Review
- γ-Secretase activity, clinical features, and biomarkers of autosomal dominant Alzheimer's disease: cross-sectional and longitudinal analysis of the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS).The Lancet. Neurology · 2024Observational
- Human brain organoids containing microglia that have arisen innately adapt to a β-amyloid challenge better than those in which microglia are integrated by co-culture.Stem cell research & therapy · 2024Article
- New precision medicine avenues to the prevention of Alzheimer's disease from insights into the structure and function of γ-secretases.The EMBO journal · 2024Review
- Formation of extramembraneProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Effects of Physical Running on Dendritic Spines and Amyloid-beta Pathology in 3xTg-AD Male Mice.Aging and disease · 2022Article
- Use of AD Informer Set compounds to explore validity of novel targets in Alzheimer's disease pathology.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- The Aβ(1-38) peptide is a negative regulator of the Aβ(1-42) peptide implicated in Alzheimer disease progression.Scientific reports · 2021Article
- Unraveling the complexity of γ-secretase.Seminars in cell & developmental biology · 2020Review
- [Progress on loss-of-function hypothesis of presenilin-1 mutations in Alzheimer diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Article
- Side-by-side comparison of Notch- and C83 binding to γ-secretase in a complete membrane model at physiological temperature.RSC advances · 2020Article
- Aβ43-producing PS1 FAD mutants cause altered substrate interactions and respond to γ-secretase modulation.EMBO reports · 2020Article
- Alzheimer's Disease: The Role of Mutations in Protein Folding.Advances in experimental medicine and biology · 2020Article
- Selective Neuronal Death in Neurodegenerative Diseases: The Ongoing Mystery.The Yale journal of biology and medicine · 2019Review
- Structure and dynamics of γ-secretase with presenilin 2 compared to presenilin 1.RSC advances · 2019Article
- The single cell origin of sporadic Alzheimer's disease: A developmental biallelic somatic mutation model.Journal of Alzheimer's disease reportsArticle
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Missense mutations in presenilin 1 cause early onset familial Alzheimer's disease in a way that is not understood. Increased Aβ42/Aβ40 ratios are the most consistent biochemical phenotype of such mutations in cultured cells and in vivo, and are thus considered central to the amyloid hypothesis. Previously, an inverse relation has been observed between the Aβ42/Aβ40 ratio of such mutants and the clinical age of symptom onset in patients carrying the mutation. However, a recent extensive study by Sun et al. of assayed presenilin 1 mutants concluded that such a relationship is not evident. To reconcile the disagreement, three different clinical datasets were compared directly with the data by Sun et al. After considering data noise and measurement uncertainty, we find a clear and highly significant inverse correlation between the Aβ42/Aβ40 ratio and the clinical age of onset in all three datasets even without removing noisy single- and double-patient data. With these data removed, the correlation coefficients increase further. The probability that these relationships are coincidental are approximately 0.1%.
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