Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease originating partly from amyloid β protein-induced synaptic failure. As damaging of noradrenergic neurons in the locus coeruleus (LC) occurs at the prodromal stage of AD, activation of adrenergic receptors could serve as the first line of defense against the onset of the disease. Activation of β2 -ARs strengthens long-term potentiation (LTP) and synaptic activity, thus improving learning and memory. Physical stimulation of animals exposed to an enriched environment (EE) leads to the activation of β2 -ARs and prevents synaptic dysfunction. EE also suppresses neuroinflammation, suggesting that β2 -AR agonists may play a neuroprotective role. The β2 -AR agonists used for respiratory diseases have been shown to have an anti-inflammatory effect. Epidemiological studies further support the beneficial effects of β2 -AR agonists on several neurodegenerative diseases. Thus, I propose that β2 -AR agonists may provide therapeutic value in combination with novel treatments for AD.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
