TY - JOUR T1 - α-Synuclein modulates tau spreading in mouse brains. AU - Bassil,Fares, AU - Meymand,Emily S, AU - Brown,Hannah J, AU - Xu,Hong, AU - Cox,Timothy O, AU - Pattabhiraman,Shankar, AU - Maghames,Chantal M, AU - Wu,Qihui, AU - Zhang,Bin, AU - Trojanowski,John Q, AU - Lee,Virginia M-Y, PY - 2019/11/20/received PY - 2020/03/12/revised PY - 2020/07/24/accepted PY - 2020/10/22/entrez PY - 2020/10/23/pubmed PY - 2021/8/31/medline JF - The Journal of experimental medicine JO - J Exp Med VL - 218 IS - 1 N2 - α-Synuclein (α-syn) and tau aggregates are the neuropathological hallmarks of Parkinson's disease (PD) and Alzheimer's disease (AD), respectively, although both pathologies co-occur in patients with these diseases, suggesting possible crosstalk between them. To elucidate the interactions of pathological α-syn and tau, we sought to model these interactions. We show that increased accumulation of tau aggregates occur following simultaneous introduction of α-syn mousepreformed fibrils (mpffs) and AD lysate-derived tau seeds (AD-tau) both in vitro and in vivo. Interestingly, the absence of endogenous mouse α-syn in mice reduces the accumulation and spreading of tau, while the absence of tau did not affect the seeding or spreading capacity of α-syn. These in vivo results are consistent with our in vitro data wherein the presence of tau has no synergistic effects on α-syn. Our results point to the important role of α-syn as a modulator of tau pathology burden and spreading in the brains of AD, PDD, and DLB patients. SN - 1540-9538 UR - https://www.unboundmedicine.com/medline/citation/33091110/α_Synuclein_modulates_tau_spreading_in_mouse_brains_ DB - PRIME DP - Unbound Medicine ER -