Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming III

ABSTRACT: Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming III

PROVIDER: PRJNA1111938 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29044370_1.fastq.gz	Fastqsanger.gz
	SRR29044370_2.fastq.gz	Fastqsanger.gz
	SRR29044371_1.fastq.gz	Fastqsanger.gz
	SRR29044371_2.fastq.gz	Fastqsanger.gz
	SRR29044372_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming

Project description:Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming

| PRJNA1063270 | ENA

Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming III

Project description:Late-onset Alzheimer’s disease (LOAD) is the most common form of AD. However, modeling sporadic LOAD, without clear genetic predispositions, to capture hallmark neuronal pathologies such as extracellular amyloid-β (Aβ) plaque deposition, intracellular tau tangles, and neuronal loss, remains an unmet need. Here, we demonstrate that neurons generated by microRNA-based direct reprogramming of fibroblasts from patients affected by autosomal dominant AD (ADAD) and LOAD in a three-dimensional (3D) environment, effectively recapitulate key neuropathological features of AD without additional cellular or genetic insults. These LOAD neurons exhibit Aβ-dependent neurodegeneration, as treatment with β- or γ-secretase inhibitors before (but not subsequent to) Aβ deposit formation mitigated neuronal death. Moreover, inhibiting age-associated retrotransposable elements (RTEs) in LOAD neurons reduced both Ab deposition and neurodegeneration. Our study underscores the efficacy of modeling late-onset neuropathology of LOAD through high-efficiency microRNA-based neuronal reprogramming.

2024-08-05 | GSE267613 | GEO

Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming II

Project description:Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming II

| PRJNA1064158 | ENA

Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming

2024-08-05 | GSE252932 | GEO

Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming II

2024-08-05 | GSE253174 | GEO

Genetic Consortium for Late Onset Alzheimer's Disease 6K

Project description:Genetic Consortium for Late Onset Alzheimer's Disease 6K

| PRJNA75441 | ENA

Human iPSC-based Modeling of Late-Onset Disease using Progerin-induced Aging

Project description:Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) sets their identity back to an embryonic age. This presents a fundamental hurdle for modeling late-onset disorders using iPSC-derived cells. We therefore developed a strategy to induce age-like features in multiple iPSC-derived lineages and tested its impact on modeling Parkinson’s disease (PD). We first describe markers that predict fibroblast donor age and observed the loss of these age-related markers following iPSC induction and re-differentiation into fibroblasts. Remarkably, age-related markers were readily induced in iPSC-derived fibroblasts or neurons following exposure to progerin including dopamine neuron-specific phenotypes such as neuromelanin accumulation. Induced aging in PD-iPSC-derived dopamine neurons revealed disease phenotypes requiring both aging and genetic susceptibility such as frank dendrite degeneration, progressive loss of tyrosine-hydroxylase expression and enlarged mitochondria or Lewy body-precursor inclusions. Our study presents a strategy for inducing age-related cellular properties and enables the modeling of late-onset disease features. Induced pluripotent stem cell-derived midbrain dopamine neurons from a young and old donor overexpressing either GFP or Progerin.

2014-01-23 | E-GEOD-52431 | biostudies-arrayexpress

Cortical hypermethylation across an extended region spanning the HOXA gene cluster on chromosome 7 is robustly associated with Alzheimer's disease neuropathology

Project description:Alzheimer's disease is a progressive neurodegenerative disorder that is hypothesized to involve epigenetic dysfunction. We undertook an epigenome-wide association study across three independent brain tissue cohorts (total n = 999) to identify differential DNA methylation associated with neuropathology in the superior temporal gyrus and prefrontal cortex. We present robust evidence for elevated DNA methylation associated with AD neuropathology across an extended region spanning the HOXA gene cluster on chromosome 7. Prefrontal cortex and superior temporal gyrus tissue from 147 individuals with varying levels of AD pathology. DNA modifications for these samples were quantified using the Illumina Infinium Human 450K Methylation Array.

2016-08-01 | E-GEOD-80970 | biostudies-arrayexpress

Human iPSC-based Modeling of Late-Onset Disease using Progerin-induced Aging

2014-01-23 | GSE52431 | GEO