Human recombinant tau and human recombinant α-synuclein fibrillar species can cross-seed efficiently in mouse models of tauopathy and synucleinopathy and copolymers of tau and α-synuclein fibrils were efficient in potentiating central nervous system (CNS) transmission of induced tau pathology but not synucleinopathy.
Why this matters
In patients with Alzheimer’s disease (AD), the presence of mixed pathologies of tau and α-synuclein is associated with a higher risk of dementia. Previous research shows that these mixed pathologies present as co-aggregates, suggesting that this pathological effect may occur as a result of interaction between these proteins.
Investigating how cross-seeding of tau and α-synuclein can influence proteinopathy can help to aid the understanding of the etiology of mixed pathologies in AD type dementias.