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Tau pathology and neurodegeneration in key prefrontal and subcortical brain regions may increase the risk of developing agitation in Alzheimer’s dementia.1 Specifically, agitation in Alzheimer’s dementia may reflect an imbalance between top-down executive control (i.e., hypoactivity in prefrontal regions) and bottom-up emotional drive (i.e., hyperactivity in subcortical regions including the amygdala).1 Moreover, agitation in Alzheimer’s dementia is associated with noradrenergic, serotonergic, and dopaminergic system dysfunction in brain circuits mediating the balance between executive control and emotional drive.2,3 In this presentation, the speakers will review the loss of behavior regulation and the role of the monoamine system in the pathophysiology of agitation associated with Alzheimer’s Dementia.
References:
1. Rosenberg, P.B., et al. Mol Aspects Med. 2015; 43-44: 25-37.
2. Jacobs, H.I., et al. Mol Psychiatry. 2021; 26(3): 897-906.
3. Lanctôt, K.L., et al. J Neuropsychiatry Clin Neurosci. 2001; 13(1): 5-21.
Senior Medical Science Liaison, CNS
Medical Science Liaison
Speakers Dennis Sholler, PhD and Justin Wimmer, PharmD are employees of Otsuka Pharmaceutical Development & Commercialization, Inc. (OPDC)
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