parkinsonsnewstoday.com/202...
The spread of alpha-synuclein aggregates in the brain is dependent on a protein receptor called TLR2, and also a transcription factor called NF-KB, a study indicates.
Blocking these proteins — which may be done with medications inhaled through the nose — may be a useful therapeutic approach in Parkinson’s disease and other conditions characterized by alpha-synuclein aggregates, its findings suggest.
The study, “Selective targeting of the TLR2/MyD88/NF-κB pathway reduces α-synuclein spreading in vitro and in vivo,” was published in Nature Communications.
Allergy drug Montelukast (aka Singulair) reduced alpha synuclein load in mice genetically engineered to over produce alpha synuclein
Nano-plastics affect a specific protein found in the brain, causing changes linked to Parkinson’s disease and other types of dementia.
SoPD blog post from Simon Stott: ADepTing to the UCB-Novartis deal
Effect of Dietary Ketosis On Alpha-Synuclein Accumulation
