Generation and characterization of a novel human iPSC line from a resilient Alzheimer's disease patient.

Stem Cell Res

Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA; The Richman Family Precision Medicine Center of Excellence in Alzheimer's Disease, Johns Hopkins Medicine and Johns Hopkins Bayview Medical Center, Baltimore, MD, USA. Electronic address:

Published: October 2020

Alzheimer's disease (AD) is a progressive neurodegenerative disease that is the major cause of dementia in older people. Here, we report the derivation of human induced pluripotent stem cells (iPSCs) from an AD patient at age of 80 who has the APOE ε4/ε4 genotype and is resilient to cognitive decline for 10 years. The iPSCs reprogrammed from the blood cells of this patient by transient expression of pluripotency genes maintain the ε4/ε4 genotype, are karyotypically normal and display typical iPSC characteristics. Upon differentiation, the iPSCs are able to differentiate into cells of the three germ layers, confirming their pluripotency.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.scr.2020.101979DOI Listing

Publication Analysis

Top Keywords

alzheimer's disease
8
ε4/ε4 genotype
8
generation characterization
4
characterization novel
4
novel human
4
human ipsc
4
ipsc resilient
4
resilient alzheimer's
4
disease patient
4
patient alzheimer's
4

Similar Publications

Translational validity of mouse models of Alzheimer's disease (AD) is variable. Because change in weight is a well-documented precursor of AD, we investigated whether diversity of human AD risk weight phenotypes was evident in a longitudinally characterized cohort of 1,196 female and male humanized APOE (hAPOE) mice, monitored up to 28 months of age which is equivalent to 81 human years. Autoregressive Hidden Markov Model (AHMM) incorporating age, sex, and APOE genotype was employed to identify emergent weight trajectories and phenotypes.

View Article and Find Full Text PDF

Lipid-induced condensate formation from the Alzheimer's Aβ peptide triggers amyloid aggregation.

Proc Natl Acad Sci U S A

January 2025

Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge CB2 1EW, United Kingdom.

The onset and development of Alzheimer's disease is linked to the accumulation of pathological aggregates formed from the normally monomeric amyloid-β peptide within the central nervous system. These Aβ aggregates are increasingly successfully targeted with clinical therapies at later stages of the disease, but the fundamental molecular steps in early stage disease that trigger the initial nucleation event leading to the conversion of monomeric Aβ peptide into pathological aggregates remain unknown. Here, we show that the Aβ peptide can form biomolecular condensates on lipid bilayers both in molecular assays and in living cells.

View Article and Find Full Text PDF

Introduction: Alzheimer's disease (AD) patients with higher educational attainment (EA) often exhibit better cognitive function. However, the relationship among EA status, AD pathology, structural brain reserve, and cognitive decline requires further investigation.

Methods: We compared cognitive performance across different amyloid beta (Aβ) positron emission tomography (A ±) statuses and EA levels (High EA/Low EA).

View Article and Find Full Text PDF

Tau Pathology Drives Disease-Associated Astrocyte Reactivity in Salt-Induced Neurodegeneration.

Adv Sci (Weinh)

January 2025

Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.

Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). Recent studies have identified a population of disease-associated astrocytes (DAA)-like astrocytes closely linked to amyloid deposition and tau pathology in an AD mouse model. However, the presence and role of these astrocytes in high-salt diet (HSD) models remain unexplored.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!