Irisin treatment lowers levels of phosphorylated tau in the hippocampus of pre-symptomatic female but not male htau mice.

Title

Irisin treatment lowers levels of phosphorylated tau in the hippocampus of pre-symptomatic female but not male htau mice.

Creator

Bretland KA; Lin Li; Bretland KM; Smith MA; Fleming SM; Dengler-Crish CM

Publisher

Neuropathology And Applied Neurobiology

Date

2021
2021-05-05

Description

Irisin is a hormone cleaved from fibronectin type-III domain-containing protein 5 in response to exercise and may be therapeutic in Alzheimer's disease (AD). Irisin is shown to repair damage caused by midlife cardiometabolic risk factors for AD (i.e., diabetes mellitus; hypertension), prevent neural amyloid beta aggregation and reduce neuroinflammation. However, there are no investigations of irisin's effect on AD-associated tauopathy in the brain. This study begins to address this gap in knowledge.

Subject

Transgenic htau mice that selectively develop age-related tauopathy were treated with recombinant irisin (100 µg/kg weekly i.p.) beginning at a pre-symptomatic age (4 months) to determine if irisin could prevent emergence of early neuropathology. One month later, mice were sacrificed to collect brain tissue and serum. Protein levels of ptau (serine 202), inflammatory cytokine tumour necrosis factor alpha (TNFα) and FNDC5 were quantified using capillary-based western blotting (Wes).

Rights

© 2021 The Authors. Neuropathology and Applied Neurobiology published by John Wiley & Sons Ltd on behalf of British Neuropathological Society.

Format

Journal Article

NEOMED College

NEOMED College of Medicine

NEOMED Department

Department of Pharmaceutical Sciences

Update Year & Number

Jan to Aug list 2021

Citation

Bretland KA; Lin Li; Bretland KM; Smith MA; Fleming SM; Dengler-Crish CM, “Irisin treatment lowers levels of phosphorylated tau in the hippocampus of pre-symptomatic female but not male htau mice.,” NEOMED Bibliography Database, accessed April 25, 2024, https://neomed.omeka.net/items/show/11866.