Serotonergic system, cognition, and BPSD in Alzheimer's disease

Saikat Chakraborty, Jack C. Lennon, Sridhar A. Malkaram, Yan Zeng, Daniel W. Fisher, Hongxin Dong*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

68 Scopus citations


Behavioral and Psychological Symptoms of Dementia (BPSD), present in almost 90% of patients with Alzheimer's Disease (AD), cause extensive impairment leading to reduced independence and inability to complete activities of daily living. Though BPSD includes a wide range of symptoms, such as agitation, aggression, disinhibition, anxiety, depression, apathy, delusions, and hallucinations. Certain BPSD in AD co-present and can be clustered into distinct domains based on their frequency of co-occurrence. As these BPSD are so pervasive in any stages of AD, the disease may be better characterized as a disorder of heterogeneous degenerative symptoms across a number of symptom domains, with the most prominent domain comprising memory and cognitive deficits. Importantly, there are no FDA-approved drugs to treat these BPSD, and new approaches must be considered to develop effective treatments for AD patients. The biogenic monoamine 5-hydroxytryptamine (5-HT), or serotonin, works as both a neurotransmitter and neuromodulator, which has been tied to cognitive decline and multiple BPSD domains. This review summarizes the evidence for specific serotonergic system alterations across some of the well-studied cognitive, behavioral, and psychiatric domains. Though differences in overall serotonergic transmission occur in AD, circuit-specific alterations in individual 5-HT receptors (5-HTRs) are likely linked to the heterogeneous presentation of BPSD in AD.

Original languageEnglish (US)
Pages (from-to)36-44
Number of pages9
JournalNeuroscience Letters
StatePublished - Jun 21 2019


  • 5-HT receptors (5-HTRs)
  • 5-hydroxytryptamine (5-HT)
  • Alzheimer's disease
  • Behavioral and psychological symptoms of dementia (BPSD)

ASJC Scopus subject areas

  • General Neuroscience


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