ArticleNeuropathology and applied neurobiology2019
The role of lysosomes and autophagosomes in frontotemporal lobar degeneration.
Article in Neuropathology and applied neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
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- Upregulating ANKHD1 in PS19 Mice Reduces Tau Phosphorylation and Mitigates Tau Toxicity-Induced Cognitive Deficits.International journal of molecular sciences · 2025Article
- Inhibiting SNX14 Alleviates Epileptic Seizures by Regulating GluA2 Degradation via the Lysosomal Pathway.Molecular neurobiology · 2025Article
- Probe-dependent Proximity Profiling (ProPPr) Uncovers Similarities and Differences in Phospho-Tau-Associated Proteomes Between Tauopathies.Molecular neurodegeneration · 2025Article
- The role of autophagy in the pathogenesis and treatment of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).Autophagy reports · 2025Review
- A toxic gain-of-function mechanism in C9orf72 ALS impairs the autophagy-lysosome pathway in neurons.Acta neuropathologica communications · 2023Article
- Neuroprotective effect of astragalin via activating PI3K/Akt-mTOR-mediated autophagy on APP/PS1 mice.Cell death discovery · 2023Article
- Human cerebral organoids - a new tool for clinical neurology research.Nature reviews. Neurology · 2022Review
- Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease.Acta neuropathologica · 2022Review
- Quantum-dot-labeled synuclein seed assay identifies drugs modulating the experimental prion-like transmission.Communications biology · 2022Article
- Article
- Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis.Neurobiology of disease · 2021Review
- Gastrodin Promotes the Survival of Random-Pattern Skin Flaps via Autophagy Flux Stimulation.Oxidative medicine and cellular longevity · 2021Article
- Tauopathies: Deciphering Disease Mechanisms to Develop Effective Therapies.International journal of molecular sciences · 2020Review
- Intracellular dynamics of Ataxin-2 in the human brains with normal and frontotemporal lobar degeneration with TDP-43 inclusions.Acta neuropathologica communications · 2020Article
- Prolonged tau clearance and stress vulnerability rescue by pharmacological activation of autophagy in tauopathy neurons.Nature communications · 2020Article
- Spleen tyrosine kinase (SYK) blocks autophagic Tau degradationThe Journal of biological chemistry · 2019Article
- The role of lysosomes and autophagosomes in frontotemporal lobar degeneration.Neuropathology and applied neurobiology · 2019Article
- Metformin Promotes the Survival of Random-Pattern Skin Flaps by Inducing Autophagy via the AMPK-mTOR-TFEB signaling pathway.International journal of biological sciences · 2019Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCell biological and genetic evidence implicate failures in degrading aggregating proteins, such as tau and TDP-43, through the autophagy or lysosomal pathways in the pathogenesis of frontotemporal lobar degeneration (FTLD).
methodsWe investigated changes in the degradative pathways in 60 patients with different pathological or genetic forms of FTLD employing immunohistochemistry for marker proteins such as lysosomal-associated membrane proteins 1 (LAMP-1) and 2 (LAMP-2), cathepsin D (CTSD) and microtubule-associated protein 1 light chain 3 alpha (LC3A). Immunostained sections were qualitatively and semi-quantitatively assessed for the appearance, distribution and intensity of staining in neurones of the dentate gyrus (DG) and CA4 region of the hippocampus, and the temporal cortex (Tcx).
resultsLower levels of neuronal LAMP-1 immunostaining were present in the DG and Tcx in FTLD-tau compared to FTLD-TDP. There was less LAMP-1 immunostaining in FTLD-tau with MAPT mutations, and FTLD-tau with Pick bodies, compared to FTLD-TDP types A and B, and less LAMP-1 immunostaining in FTLD-TDP type C than in FTLD-TDP types A and B. There was greater LAMP-1 immunostaining in GRN mutation which may reflect the underlying type A histology rather than mutation. There were no differences in neuronal LAMP-2, CTSD, EEA-1 or LC3A immunostaining between any of the five FTLD histological or four genetic groups, nor between FTLD-TDP and FTLD-tau.
conclusionsThe underlying pathological mechanism in FTLD-tau may lie with a relative deficiency of lysosomes, or defective vesicular transport, whereas the failure to clear TDP-43 aggregates may lie with lysosomal dysfunction rather than a lack of available lysosomes or degradative enzymes.
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