Associated Papers
Cytokine-induced reprogramming of human macrophages toward Alzheimer's disease-relevant molecular and cellular phenotypes in vitro.
Podleśny-Drabiniok A et al.
Cell Reports, 2025
40570367 (PubMed )
Supplement: NIHMS2099510-supplement-6.xlsx › VSQR_THP-1
The landscape of autosomal-dominant Alzheimer's disease: global distribution and age of onset.
Liu H et al.
Brain : a Journal of Neurology, 2025
39903689 (PubMed )
Supplement: awaf038_supplementary_data.zip › 2-Supplemental_Table1_AR_20250121_JLliF.pdf
Conformational Models of APP Processing by Gamma Secretase Based on Analysis of Pathogenic Mutations.
Kim M et al.
International Journal of Molecular Sciences, 2021
Aβ42/Aβ40 Ratios of Presenilin 1 Mutations Correlate with Clinical Onset of Alzheimer's Disease.
Tang N et al.
Journal of Alzheimer's Disease : Jad, 2018
30412504 (PubMed )
Supplement: sj-docx-1-alz-10.3233_jad-180829.docx
Serum neurofilament light in familial Alzheimer disease: A marker of early neurodegeneration.
Weston PSJ et al.
Neurology, 2017
29070659 (PubMed )
Supplement: supp_WNL.0000000000004667_Table_e-1.docx
Clinical phenotype and genetic associations in autosomal dominant familial Alzheimer's disease: a case series.
Ryan NS et al.
The Lancet. Neurology, 2016
Retromer and Rab2-dependent trafficking mediate PS1 degradation by proteasomes in endocytic disturbance.
Ueda N et al.
Journal of Neurochemistry, 2016
The genetics of Alzheimer's disease.
Bagyinszky E et al.
Clinical Interventions in Aging, 2014
Closely spaced multiple mutations as potential signatures of transient hypermutability in human genes.
Chen JM et al.
Human Mutation, 2009
Clinical phenotypic heterogeneity of Alzheimer's disease associated with mutations of the presenilin-1 gene.
Larner AJ et al.
Journal of Neurology, 2006
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