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SmRNA-sequencing of human post-mortem brain tissue of the frontal lobe from patients with Frontotemporal Dementia and healthy controls

ABSTRACT: Understanding the molecular mechanisms underlying frontotemporal dementia (FTD) is essential for the development of successful therapies. Systematic studies on human post-mortem brain tissue of patients with genetic subtypes of FTD are currently lacking. The Risk and Modyfing Factors of Frontotemporal Dementia (RiMod-FTD) consortium therefore has generated multi-omics datasets for genetic subtypes of FTD to identify common and distinct molecular mechanisms disturbed in disease. This experiment contains data from smRNA-sequencing of human post-mortem brain tissue of the frontal lobe from patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

INSTRUMENT(S): NextSeq 550

ORGANISM(S): Homo sapiens

SUBMITTER: Kevin Menden

PROVIDER: E-MTAB-12731 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNA-seq of human post-mortem brain tissue of the frontal lobe from patients with FTD and healthy controls

Project description:Understanding the molecular mechanisms underlying frontotemporal dementia (FTD) is essential for the development of successful therapies. Systematic studies on human post-mortem brain tissue of patients with genetic subtypes of FTD are currently lacking. The Risk and Modyfing Factors of Frontotemporal Dementia (RiMod-FTD) consortium therefore has generated multi-omics datasets for genetic subtypes of FTD to identify common and distinct molecular mechanisms disturbed in disease. This experiment contains data from RNA-sequencing of human post-mortem brain tissue of the frontal lobe from patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

2023-02-17 | E-MTAB-12647 | biostudies-arrayexpress

CAGE-seq of human post-mortem brain tissue of the frontal lobe from patients with FTD and healthy controls

Project description:Understanding the molecular mechanisms underlying frontotemporal dementia (FTD) is essential for the development of successful therapies. Systematic studies on human post-mortem brain tissue of patients with genetic subtypes of FTD are currently lacking. The Risk and Modyfing Factors of Frontotemporal Dementia (RiMod-FTD) consortium therefore has generated multi-omics datasets for genetic subtypes of FTD to identify common and distinct molecular mechanisms disturbed in disease. This experiment contains data from CAGE-sequencing of human post-mortem brain tissue of the frontal lobe from patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

2023-02-26 | E-MTAB-12646 | biostudies-arrayexpress

Methylation state of human post-mortem brain tissue from the frontal lobe of patients with Frontotemporal Dementia and healthy controls

Project description:Methylation state of human post-mortem brain tissue from the frontal lobe of patients with Frontotemporal Dementia caused by mutations in GRN, MAPT and C9orf72 and healthy controls

2023-02-01 | E-MTAB-12674 | biostudies-arrayexpress

Genome-wide DNA methylation analysis identifies epigenetic differences in Alzheimer’s disease and frontotemporal dementia in brain tissue and lymphoblastoid cell lines

Project description:We have performed methylation microarray analysis of two types of dementia, Alzheimer's disease (AD) and frontotemporal dementia (FTD), using two kind of samples, frozen brain tissue and lymphoblastoid cell lines.

2024-01-01 | E-MTAB-11975 | biostudies-arrayexpress

E-PROT-137

Project description:Distinct cell type-specific protein signatures in GRN and MAPT genetic subtypes of frontotemporal dementia

2024-06-05 | E-PROT-137 | ExpressionAtlas

Neurovascular dysfunction in GRN-associated frontotemporal dementia identified by single-nucleus RNA-sequencing of human cerebral cortex

Project description:Frontotemporal dementia (FTD) is the second most prevalent form of early-onset dementia, affecting predominantly frontal and temporal cerebral lobes. Heterozygous mutations in the progranulin gene (GRN) cause autosomal-dominant FTD (FTD-GRN), associated with TDP-43 inclusions, neuronal loss, axonal degeneration and gliosis, but FTD-GRN pathogenesis is largely unresolved. Here we report single-nucleus RNA sequencing of microglia, astrocytes and the neurovasculature from frontal, temporal and occipital cortical tissue from control and FTD-GRN brains. We show that fibroblast and mesenchymal cell numbers were enriched in FTD-GRN, and we identified disease-associated subtypes of astrocytes and endothelial cells. Expression of gene modules associated with blood–brain barrier (BBB) dysfunction was significantly enriched in FTD-GRN endothelial cells. The vasculature supportive function and capillary coverage by pericytes was reduced in FTD-GRN tissue, with increased and hypertrophic vascularization and an enrichment of perivascular T cells. Our results indicate a perturbed BBB and suggest that the neurovascular unit is severely affected in FTD-GRN.

2022-06-03 | GSE163122 | GEO

Differential gene expression in sporadic and genetic forms of Alzheimer’s disease and frontotemporal dementia in brain tissue and lymphoblastoid cell lines.

Project description:We have performed gene expression microarray analysis of two types of dementia, Alzheimer's disease (AD) and frontotemporal dementia (FTD), using two kind of samples, frozen brain tissue and lymphoblastoid cell lines.

2022-12-12 | GSE195872 | GEO

Project description:Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) represent two ends of a disease spectrum with shared clinical, genetic and pathological features. These include near ubiquitous pathological inclusions of the RNA binding protein (RBP) TDP-43, and often the presence of a GGGGCC expansion in the C9ORF72 (C9) gene. Here we show unexpectedly that the signature of hnRNP H sequestration and altered splicing of target transcripts we identified in C9ALS patients (Conlon et al. 2016) also occurs in fully half of 50 post-mortem sporadic, non-C9 ALS/FTD post-mortem brains. Furthermore, and equally surprisingly, these “like-C9” brains also contained correspondingly high amounts of insoluble TDP-43, as well as several other disease-related RBPs, and this correlates with widespread global splicing defects. Finally, we show that the like-C9 sporadic patients, like actual C9ALS patients, were much more likely to have developed FTD. We propose that these unexpected links between C9 and sporadic ALS/FTD define a common mechanism in this disease spectrum.

2018-07-13 | GSE116622 | GEO

Distinct cell type-specific protein signatures in GRN and MAPT genetic subtypes of frontotemporal dementia

Project description:INTRODUCTION: Frontotemporal dementia (FTD) is characterized by progressive atrophy of frontal and/or temporal cortices and considerable clinical, pathological, and genetic heterogeneity. METHODS: Frontal and temporal cortex tissues from FTD-GRN (n=9), FTD-MAPT (n=13), and non-demented controls (n=11) were analysed with quantitative proteomics (DIA). Expression-weighted cell type enrichment deduced the role of major brain cell types and gene ontology analysis identified distinct biological processes. FTD-MAPT data was also compared to an AD (n=10) protein signature. RESULTS: We identified brain region-specific FTD protein expression signatures. In frontal cortex of FTD-GRN, we observed immune processes in endothelial cells and mitochondrial dysregulation in neurons. In temporal cortex of FTD-MAPT, we observed dysregulated RNA processing, oligodendrocyte dysfunction, and axonal impairment. Comparison with AD indicated that alterations in RNA processing and oligodendrocyte function are distinct for FTD-MAPT. DISCUSSION: Our results indicate cell type-specific biological processes distinctive for genetic FTD subtypes. These findings may aid the development of FTD subtype-specific treatment strategies.

2022-08-12 | PXD031419 | Pride

Abnormal RNA stability in amyotrophic lateral sclerosis

Project description:Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) share key features, including accumulation of the RNA binding protein TDP-43. TDP-43 regulatesRNA homeostasis, but it remains unclear whether RNA stability is affected in these disorders. We used Bru-seq and BruChase-seq to assessgenome-wide RNA stabilityinALS patient-derived cells,demonstratingprofound destabilization of ribosomal and mitochondrial transcripts. This pattern wasrecapitulatedbyTDP-43 overexpression, suggesting a primary role for TDP-43 in RNA destabilization, and in post-mortem samples from ALS and FTD patients. Proteomics and functional studies illustrated corresponding reductionsin mitochondrial components and compensatory increasesin protein synthesis. Collectively, these observations suggest that TDP-43 deposition leads to targeted RNA instability in ALS and FTD, ultimately causing cell death by disrupting energy production and protein synthesis pathways.

2018-07-25 | GSE115310 | GEO

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