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Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency [1 month]

ABSTRACT: Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency [1 month]

PROVIDER: PRJNA890683 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21910931_1.fastq.gz	Fastqsanger.gz
	SRR21910931_2.fastq.gz	Fastqsanger.gz
	SRR21910932_1.fastq.gz	Fastqsanger.gz
	SRR21910932_2.fastq.gz	Fastqsanger.gz
	SRR21910933_1.fastq.gz	Fastqsanger.gz

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Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency.

Project description:Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency.

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Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency [1 yr]

Project description:Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency [1 yr]

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Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency [1 month]

Project description:Spinocerebellar Ataxia Autosomal Recessive 20 (SCAR20) is a rare disorder caused by mutation in the SNX14 gene. The symptoms of the disorder including coarse face, poor or lack of speech, delayed or absent of motor function, and most markedly, cerebella atrophy with Purkinje cell degeneration. SNX14 has been localized to ER and shown to play a vital role in facilitating the formation of lipid droplet and maintaining the lipid saturation balance in cell membrane. Meanwhile, it has also been localized to other subcellular organelles, including lysosome and endo-lysosome, and has been suggested to participate in the autophagy responses. However, the previous researches were performed in vitro or ex vivo, and how disrupted SNX14 led to Purkinje cell degeneration in the SCAR20 cerebella in vivo remained unexplored. Here, we report the first animal model that manifested the SCAR20 symptoms, by introducing a 1bp deletion in Snx14 in mice via CRISPR-Cas9. We performed RNAseq to analyse the pathway changes caused by Snx14 KO.

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Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency.

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Altered lipid homeostasis underlies selective neurodegeneration in SNX14 deficiency [1 yr]

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Neuronal ApoE Upregulates MHC-I Expression to Drive Selective Neurodegeneration in Alzheimer’s Disease

Project description:Selective neurodegeneration is a critical causal factor in Alzheimer’s disease (AD); however, the mechanisms that lead some neurons to perish while others remain resilient are unknown. We sought potential drivers of this selective vulnerability using single-nucleus RNA sequencing and discovered that apoE expression level is a substantial driver of neuronal variability. Strikingly, neuronal expression of apoE—which has a robust genetic linkage to AD—correlated strongly, on a cell-by-cell basis, with immune response pathways in neurons in the brains of wildtype mice, human apoE knock-in mice, and humans with or without AD. Elimination or over-expression of neuronal apoE revealed a causal relationship between apoE expression, neuronal MHC-I expression, Tau pathology, and neurodegeneration. Functional reduction of MHC-I ameliorated Tau pathology in apoE4-expressing primary neurons and in mouse hippocampi expressing pathological Tau. These findings suggest a mechanism linking neuronal apoE expression to MHC-I expression and, subsequently, to Tau pathology and selective neurodegeneration.

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