| Autor: |
Mazzotta GM; Department of Biology, University of Padova, 35131 Padova, Italy., Ceccato N; Department of Biology, University of Padova, 35131 Padova, Italy., Conte C; Department of Pharmaceutical Sciences, University of Perugia, 06100 Perugia, Italy. |
| Jazyk: |
angličtina |
| Zdroj: |
Cells [Cells] 2023 Apr 24; Vol. 12 (9). Date of Electronic Publication: 2023 Apr 24. |
| DOI: |
10.3390/cells12091231 |
| Abstrakt: |
The misfolding and subsequent abnormal accumulation and aggregation of α-Synuclein (αSyn) as insoluble fibrils in Lewy bodies and Lewy neurites is the pathological hallmark of Parkinson's disease (PD) and several neurodegenerative disorders. A combination of environmental and genetic factors is linked to αSyn misfolding, among which neuroinflammation is recognized to play an important role. Indeed, a number of studies indicate that a Toll-like receptor (TLR)-mediated neuroinflammation might lead to a dopaminergic neural loss, suggesting that TLRs could participate in the pathogenesis of PD as promoters of immune/neuroinflammatory responses. Here we will summarize our current understanding on the mechanisms of αSyn aggregation and misfolding, focusing on the contribution of TLRs to the progression of α-synucleinopathies and speculating on their link with the non-motor disturbances associated with aging and neurodegenerative disorders. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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