Background: Alzheimer's Disease (AD) manifests early in the olfactory system, yet its precise role in the pathophysiology of AD remains elusive. This study aims to elucidate the progression of olfactory dysfunction in AD by investigating the dysregulation of the adenosine 2A receptor (A2AR) and its potential involvement in the formation of abnormal plaques and tangles. A2AR plays a pivotal role in modulating synaptic transmission and neuroinflammation by regulating both neurons and glial cells.
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