Pre-clinical support for a pathway for gut-to-brain propagation of misfolded α-syn
 

ScienceDaily article:
"Pre-clinical study suggests Parkinson's could start in gut endocrine cells:
- protein linked to Parkinson's could spread from gut to nervous system"

Pre-clinical study suggests Parkinson's could start in gut endocrine cells: Protein linked to Parkinson's could spread from gut to nervous system -- ScienceDaily

Open-access research paper:
"Alpha-Synuclein in gut endocrine cells and its implications for Parkinson's disease", Rashmi Chandra, Annie Hiniker, Yien-Ming Kuo, Robert L. Nussbaum, Rodger A. Liddle. JCI Insight, 2017; 2 (12) DOI: 10.1172/jci.insight.92295

JCI Insight -
α-Synuclein in gut endocrine cells and its implications for Parkinson’s disease

(hat tip to aspergerian at HU for the links)

Thanks jeffreyn - it looks like a very impressive paper to me.

As an aside, JCI (the parent of JCI Insight) is one of the most respected biomedical journals, with an impact factor of >12.

Because of that, I doubt that poor-quality work will get published in JCI Insight.

alpha-synuclein curcumen
 

Curcumin Treatment Improves Motor Behavior in α-Synuclein Transgenic Mice

Effect of curcumin analogs onα-synuclein aggregation and cytotoxicity. - PubMed - NCBI

The curry spice curcumin plays a protective role in mouse models of neurodegenerative diseases, and can also directly modulate aggregation of α-synuclein protein in vitro, yet no studies have described the interaction of curcumin and α-synuclein in genetic synucleinopathy mouse models. Here we examined the effect of chronic and acute curcumin treatment in the Syn-GFP mouse line, which overexpresses wild-type human α-synuclein protein. We discovered that curcumin diet intervention significantly improved gait impairments and resulted in an increase in phosphorylated forms of α-synuclein at cortical presynaptic terminals. Acute curcumin treatment also caused an increase in phosphorylated α-synuclein in terminals, but had no direct effect on α-synuclein aggregation, as measured by in vivo multiphoton imaging and Proteinase-K digestion. Using LC-MS/MS, we detected ~5 ng/mL and ~12 ng/mL free curcumin in the plasma of chronic or acutely treated mice, with a glucuronidation rate of 94% and 97%, respectively. Despite the low plasma levels and extensive metabolism of curcumin, these results show that dietary curcumin intervention correlates with significant behavioral and molecular changes in a genetic synucleinopathy mouse model that mimics human disease.