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autophagy-lysosome pathway

Candidate: concept label1 source documents3 linked claims
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Aliases

ALP

Extracted Explainers

What the tool is doing

The autophagy-lysosome pathway is presented as the protein-homeostasis pathway whose dysfunction is discussed across recent C9orf72 studies. The review frames it as altered at multiple levels in ALS-FTD.

Source 1DOIPubMed

What problem it solves

As a concept label, it helps organize the review's mechanistic synthesis around degradation and lysosomal homeostasis defects.

Source 1DOIPubMed

What it does not solve

The abstract does not identify it as a discrete therapeutic or engineering tool.

Source 1DOIPubMed

Alternatives

The abstract also mentions the ubiquitin-proteasome system as related protein-homeostasis context.

Source 1DOIPubMed

Evidence Snippets

In this review, we discuss the effects of the C9orf72 HRE in the autophagy-lysosome pathway based on various recent findings.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1disease mechanism synthesissupports2021Source 1DOIPubMed

Alterations in protein homeostasis are presented as one of the root causes of C9orf72-associated ALS-FTD pathogenesis.

Quoted textsource-backed
In addition, several recent studies point toward alterations in protein homeostasis as one of the root causes of the disease pathogenesis.
Claim 2pathogenesis mechanismsupports2021Source 1DOIPubMed

C9orf72 hexanucleotide repeat expansions, toxic repeat RNA, DPR production, and reduced C9orf72 expression are proposed contributors to ALS-FTD pathogenesis.

Quoted textsource-backed
Though the mechanisms by which HREs cause toxicity is not clear, the toxic gain of function due to transcribed HRE RNA or dipeptide repeat proteins (DPRs) produced by repeat-associated non-AUG translation together with a reduction in C9orf72 expression are proposed as the contributing factors for disease pathogenesis in ALS and FTD.
Claim 3synergy mechanismsupports2021Source 1DOIPubMed

Dysfunction of the autophagy-lysosome pathway is suggested to synergize with toxicity from C9orf72 repeat RNA and DPRs to drive ALS-FTD pathogenesis.

Quoted textsource-backed
We suggest that dysfunction of the autophagy-lysosome pathway synergizes with toxicity from C9orf72 repeat RNA and DPRs to drive disease pathogenesis.