Work

Glucocorticoids, synaptic plasticity and Alzheimer's disease

Year: 2022

Type: review

Abstract: How excessive stress and cortisol exposure predispose people to clinical Alzheimer's disease (AD) is a matter of great potential medical impact. We discuss recent findings regarding the mechanism of persistent disruption of synaptic plasticity and related cognition caused by hypothalamic–pituitary–adrenal (HPA) axis dysregulation in this context. Growing evidence supports the view that in addition to the pathogenic proteins amyloid beta and tau driving HPA and hence synaptic plasticity disruption, excess glucocorticoid receptor activation promotes amyloidosis and tauopathy-mediated synaptotoxicity. The critical role of glia-mediated pro-inflammatory processes in the impairment of synaptic and cognitive function by stress is also delineated. Combining (non)-pharmacological interventions that target glucocorticoid-synaptic plasticity pathways with more classical anti-tau and anti-amyloid strategies to treat early AD prior to dementia onset certainly warrants further investigation.

Source: Current Opinion in Endocrine and Metabolic Research

DOI: 10.1016/j.coemr.2022.100365

Authors: Igor Klyubin, Tomas Ondrejcak, Neng-Wei Hu, Michael J. Rowan

Institutions: Trinity College Dublin, Zhengzhou University

Language: English

Topic: Alzheimer's disease research and treatments

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $3,900