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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.