ReviewFrontiers in synaptic neuroscience2020
Histone Deacetylase 6 and the Disease Mechanisms of α-Synucleinopathies.
Review in Frontiers in synaptic neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Chemical Epigenetics: Small Molecules Targeting Chromatin Modifiers in Disease Modulation.Cell biochemistry and biophysics · 2026Review
- TARDBP as a regulator of HIV-1 assembly and infection: a review of targeting the viral capsid precursor Pr55Gag and limiting viral core entry.Cell communication and signaling : CCS · 2026Review
- Histone deacetylase 6: A new player in oxidative stress‑associated disorders and cancers (Review).International journal of molecular medicine · 2025Review
- Review
- Revamping Parkinson's disease therapy using PLGA-based drug delivery systems.NPJ Parkinson's disease · 2025Review
- Perillaldehyde Improves Parkinson-Like Deficits by Targeting G3BP Mediated Stress Granule Assembly in Preclinical Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Regulation of HDAC6 Catalytic Activity in Cancer: The Role of Post-Translational Modifications and Protein-Protein Interactions.International journal of molecular sciences · 2025Review
- Canonical and noncanonical autophagy: involvement in Parkinson's disease.Frontiers in cell and developmental biology · 2025Review
- Changes in α-Synuclein Posttranslational Modifications in an AAV-Based Mouse Model of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Acetylated α-Tubulin and α-Synuclein: Physiological Interplay and Contribution to α-Synuclein Oligomerization.International journal of molecular sciences · 2023Article
- Alpha synuclein post translational modifications: potential targets for Parkinson's disease therapy?Frontiers in molecular neuroscience · 2023Review
- Transactive Response DNA-Binding Protein (TARDBP/TDP-43) Regulates Cell Permissivity to HIV-1 Infection by Acting on HDAC6.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
2 authors.
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Abstract
The abnormal accumulation of α-Synuclein (α-Syn) is a prominent pathological feature in a group of diseases called α-Synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). The formation of Lewy bodies (LBs) and glial cytoplasmic inclusions (GCIs) in neurons and oligodendrocytes, respectively, is highly investigated. However, the molecular mechanisms behind α-Syn improper folding and aggregation remain unclear. Histone deacetylase 6 (HDAC6) is a Class II deacetylase, containing two active catalytic domains and a ubiquitin-binding domain. The properties of HDAC6 and its exclusive cytoplasmic localization allow HDAC6 to modulate the microtubule dynamics, acting as a specific α-tubulin deacetylase. Also, HDAC6 can bind ubiquitinated proteins, facilitating the formation of the aggresome, a cellular defense mechanism to cope with higher levels of misfolded proteins. Several studies report that the aggresome shares similarities in size and composition with LBs and GCIs. HDAC6 is found to co-localize with α-Syn in neurons and in oligodendrocytes, together with other aggresome-related proteins. The involvement of HDAC6 in several neurodegenerative diseases is already under discussion, however, the results obtained by modulating HDAC6 activity are not entirely conclusive. The main goal of this review is to summarize and critically discuss previous
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