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

Stimulation of mTOR-independent autophagy and mitophagy by rilmenidine exacerbates the phenotype of transgenic TDP-43 mice.

Neurobiology of disease - 1 Jul 2021

Perera Nirma D, Tomas Doris, Wanniarachchillage Nayomi, Cuic Brittany, Luikinga Sophia J, Rytova Valeria, Turner Bradley J

Abstract excerpt

Autophagy, which mediates the delivery of cytoplasmic substrates to the lysosome for degradation, is essential for maintaining proper cell homeostasis in physiology, ageing, and disease. There is increasing evidence that autophagy is defective in neurodegenerative disorders, including motor neurons affected in amyotrophic lateral sclerosis (ALS). Restoring impaired autophagy in motor neurons may therefore...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to Antihypertensive Agents

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Autophagy

Share to DNA-Binding Proteins

Share to Mice, Inbred C57BL

Share to Mice, Transgenic

Share to Mitophagy

Share to TOR Serine-Threonine Kinases

Source

Identifiers

PMID: 33798740
DOI: 10.1016/j.nbd.2021.105359

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Stimulation of mTOR-independent autophagy and mitophagy by rilmenidine exacerbates the phenotype of transgenic TDP-43 mice.PMID 33798740Read ↗

Rilmenidine attenuates toxicity of polyglutamine expansions in a mouse model of Huntington's diseaseSemantic proximity Read ↗

A robust TDP-43 knock-in mouse model of ALSSemantic proximity Read ↗

Hemizygous deletion of Tbk1 worsens neuromuscular junction pathology in TDP-43G298S transgenic mice.Semantic proximity Read ↗

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanismSemantic proximity Read ↗

Distinct roles for motor neuron autophagy early and late in the SOD1 G93A mouse model of ALSSemantic proximity Read ↗

Targeting autophagy in ALS: a complex mission.Semantic proximity Read ↗

Chronic Rapamycin administration via drinking water mitigates the pathological phenotype in a Krabbe disease mouse model through autophagy activation.Semantic proximity Read ↗

Loss of TBK1 activity leads to TDP-43 proteinopathy through lysosomal dysfunction in human motor neuronsSemantic proximity Read ↗

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism.Semantic proximity Read ↗

Aberrant dynein function promotes TDP-43 aggregation and upregulation of p62 in male mice harboring transgenic human TDP-43Semantic proximity Read ↗

Inhibition of autophagy delays motoneuron degeneration and extends lifespan in a mouse model of spinal muscular atrophy.Semantic proximity Read ↗

Motor neuron-specific disruption of proteasomes, but not autophagy, replicates amyotrophic lateral sclerosis.Semantic proximity Read ↗

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