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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE315586 | GEO | 2026/01/05

REPOSITORIES: GEO

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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [RNA-seq]

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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [snRNAseq/snATACseq multiomics]

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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis

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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [RNA-seq]

Project description:Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [RNA-seq]

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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [snRNAseq/snATACseq multiomics]

Project description:Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [snRNAseq/snATACseq multiomics]

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Differential Cellular Mechanisms Underlie Language and Executive Decline in Amyotrophic Lateral Sclerosis [Visium spatial transcriptomics]

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Amyotrophic lateral sclerosis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Role of Neuroinflammation in Amyotrophic Lateral Sclerosis: Cellular Mechanisms and Therapeutic Implications.

Project description:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects upper motor neurons (MNs) comprising the corticospinal tract and lower MNs arising from the brain stem nuclei and ventral roots of the spinal cord, leading to fatal paralysis. Currently, there are no effective therapies for ALS. Increasing evidence indicates that neuroinflammation plays an important role in ALS pathogenesis. The neuroinflammation in ALS is characterized by infiltration of lymphocytes and macrophages, activation of microglia and reactive astrocytes, as well as the involvement of complement. In this review, we focus on the key cellular players of neuroinflammation during the pathogenesis of ALS by discussing not only their detrimental roles but also their immunomodulatory actions. We will summarize the pharmacological therapies for ALS that target neuroinflammation, as well as recent advances in the field of stem cell therapy aimed at modulating the inflammatory environment to preserve the remaining MNs in ALS patients and animal models of the disease.

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