Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Aging-Dependent Altered Transcriptional Programs Underlie Activity Impairments in Human C9orf72-Mutant Motor Neurons

14 Jun 2022

Abstract excerpt

Amyotrophic Lateral Sclerosis (ALS) is an incurable neurodegenerative disease characterized by dysfunction and loss of upper and lower motor neurons (MN). Despite several studies identifying drastic alterations affecting synaptic composition and functionality in different experimental models, the specific contribution of impaired activity to the neurodegenerative processes observed in ALS-related MN remains...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis Research
Share to Cholinesterase and Neurodegenerative Diseases
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 35774867
DOI: 10.3389/fnmol.2022.894230

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Aging-Dependent Altered Transcriptional Programs Underlie Activity Impairments in Human C9orf72-Mutant Motor NeuronsPMID 35774867Read ↗

Dysregulation of synaptic transcripts underlies network abnormalities in ALS patient-derived motor neuronsSemantic proximity Read ↗

Dysregulation of synaptic transcripts underlies network abnormalities in ALS patient-derived motor neurons.Semantic proximity Read ↗

Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction.Semantic proximity Read ↗

Neuronal Activity-Dependent Gene Dysregulation in <i>C9orf72</i> i <sup>3</sup> Neuronal Models of ALS/FTD PathogenesisSemantic proximity Read ↗

Electrophysiological Phenotype Characterization of Human iPSC-Derived Neuronal Cell Lines by Means of High-Density Microelectrode ArraysSemantic proximity Read ↗

Electrophysiological Phenotype Characterization of Human iPSC-Derived Neuronal Cell Lines by Means of High-Density Microelectrode Arrays.Semantic proximity Read ↗

Intrinsic membrane hyperexcitability of amyotrophic lateral sclerosis patient-derived motor neurons.Semantic proximity Read ↗

Synaptic disruption and CREB‐regulated transcription are restored by K+ channel blockers in ALSSemantic proximity Read ↗

A mitochondrial tipping point couples early hyperexcitability to late-stage failure in patient-derived ALS motor neuronsSemantic proximity Read ↗

Patient-Derived <i>PSEN1</i> Cerebral Organoids Revealed Parallel Development of Amyloid-β Accumulation and Network DysfunctionSemantic proximity Read ↗

Mitochondrial dysfunction impairs human neuronal development and reduces neuronal network activity and synchronicitySemantic proximity Read ↗

Early pathogenesis in the adult-onset neurodegenerative disease amyotrophic lateral sclerosis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.