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Molecular characterization of selectively vulnerable neurons in Alzheimer’s Disease

ABSTRACT: Molecular characterization of selectively vulnerable neurons in Alzheimer’s Disease

PROVIDER: PRJNA615180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11422700.fastq.gz	Fastqsanger.gz
	SRR11422701.fastq.gz	Fastqsanger.gz
	SRR11422702.fastq.gz	Fastqsanger.gz
	SRR11422703.fastq.gz	Fastqsanger.gz
	SRR11422704.fastq.gz	Fastqsanger.gz

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Molecular characterization of selectively vulnerable neurons in Alzheimer’s Disease

Project description:Alzheimer’s disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown. To identify and characterize selectively vulnerable neuronal populations, we used single-nucleus RNA sequencing to profile the caudal entorhinal cortex and the superior frontal gyrus – brain regions where neurofibrillary inclusions and neuronal loss occur early and late in AD, respectively – from individuals spanning the neuropathological progression of AD. We identified RORB as a marker of selectively vulnerable excitatory neurons in the entorhinal cortex, and subsequently validated their depletion and selective susceptibility to neurofibrillary inclusions during disease progression using quantitative neuropathological methods. We also discovered an astrocyte subpopulation, likely representing reactive astrocytes, characterized by decreased expression of genes involved in homeostatic functions. Our characterization of selectively vulnerable neurons in AD paves the way for future mechanistic studies of selective vulnerability and potential therapeutic strategies for enhancing neuronal resilience. The brain tissue used in this study were sourced from the Biobank for Aging Studies (LIM-22) in the Department of Pathology at the University of Sao Paulo, as well as from the Neurodegenerative Diseases Brain Bank in the Memory and Aging Center at the University of California, San Francisco. Detailed neuropathological, clinical and genetic data are available under request. Please contact gerolab@gmail.com and lea.grinberg@ucsf.edu.

2020-04-05 | GSE147528 | GEO

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invivo]

Project description:Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. The present GEO entry corresponds to cell-type specific RNA-sequencing of ECII neurons in vivo 1 week after DEK silencing using AAV vectors.

2022-05-22 | GSE203366 | GEO

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [chromatin]

Project description:Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. Since DEK is a chromatin modulator, we investigated the genomic location of a few histone marks in DEK silenced cells using the CUT&TAG approach, as well as Chromatin Accessibility using ATAC-seq

2022-05-22 | GSE203364 | GEO

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invitro]

Project description:Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer’s disease. We used a data-driven functional genomics approach to model ECII neurons in silico that led us to the prediction that the proto-oncogene DEK is a driver of tau pathology in these neurons. In order to understand the function of DEK in vulnerable neurons, we modulated its expression in ECII neurons in vitro and in vivo in the mouse. The present GEO entry includes all of the data we collected from DEK-silenced and DEK-overexpressing ECneurons in vitro and in vivo.

2022-05-22 | GSE203365 | GEO

Molecular characterization of selectively vulnerable neurons in Alzheimer's disease.

Project description:Alzheimer's disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown. To identify and characterize selectively vulnerable neuronal populations, we used single-nucleus RNA sequencing to profile the caudal entorhinal cortex and the superior frontal gyrus-brain regions where neurofibrillary inclusions and neuronal loss occur early and late in AD, respectively-from postmortem brains spanning the progression of AD-type tau neurofibrillary pathology. We identified RORB as a marker of selectively vulnerable excitatory neurons in the entorhinal cortex and subsequently validated their depletion and selective susceptibility to neurofibrillary inclusions during disease progression using quantitative neuropathological methods. We also discovered an astrocyte subpopulation, likely representing reactive astrocytes, characterized by decreased expression of genes involved in homeostatic functions. Our characterization of selectively vulnerable neurons in AD paves the way for future mechanistic studies of selective vulnerability and potential therapeutic strategies for enhancing neuronal resilience.

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The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons.

Project description:The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons.

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The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [chromatin]

Project description:The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [chromatin]

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The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invitro]

Project description:The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invitro]

| PRJNA839696 | ENA

The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invivo]

Project description:The proto-oncogene DEK regulates neuronal excitability and tau accumulation in Alzheimer’s disease vulnerable neurons [RNA-seq_invivo]

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Single-cell transcriptomics unveils molecular signatures of neuronal vulnerability in a mouse model of prion disease that overlap with Alzheimer’s disease

Project description:Understanding why certain neurons are more sensitive to dysfunction and death caused by misfolded proteins could provide therapeutically relevant insights into neurodegenerative disorders. Here, we harnessed single-cell transcriptomics to examine live neurons isolated from prion-infected female mice, aiming to identify and characterize prion-vulnerable neuronal subsets. Our analysis revealed distinct transcriptional responses across neuronal subsets, with a consistent pathway-level depletion of synaptic gene expression in damage-vulnerable neurons. By scoring neuronal damage based on the magnitude of depleted synaptic gene expression, we identified a diverse spectrum of prion-vulnerable glutamatergic, GABAergic, and medium spiny neurons. Comparison between prion-vulnerable and resistant neurons highlighted baseline gene expression differences that could influence neuronal vulnerability. For instance, the neuroprotective cold-shock protein Rbm3 exhibited higher baseline gene expression in prion-resistant neurons and was robustly upregulated across diverse neuronal classes upon prion infection. We also identified vulnerability-correlated transcripts that overlapped between prion and Alzheimer’s disease. Our findings not only demonstrate the potential of single-cell transcriptomics to identify damage-vulnerable neurons, but also provide molecular insights into neuronal vulnerability and highlight commonalties across neurodegenerative disorders.

2024-10-25 | GSE249382 | GEO

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