Abstract
Neuropsychiatric symptoms (NPS) including behavioral and psychiatric symptoms are common in the dementia stages of Alzheimer's disease (AD) and are associated with poorer outcomes in cognition, functional states, quality of life, and accelerated progression to severe dementia or death. NPS are also increasingly observed in the mild cognitive impairment stage of AD and may predict incipient dementia. As such, there is an emerging conceptual framework, which support NPS as early non-cognitive symptoms of dementia. [18F]fluorodeoxyglucosepositron emission tomography is a technique that is sensitive in detecting resting metabolism associated with NPS in neuropsychiatric conditions, and there is a growing body of literature evaluating the role of NPS as early indicators of brain metabolic dysfunctions in AD. In this mini-review, we examine the frequency and associations of NPS with metabolic dysfunction in the AD continuum, including preclinical, prodromal, and dementia stages of AD. We will also present the validated neurobehavioral syndrome, mild behavioral impairment describes the later life emergence of sustained NPS as an at-risk state for incident cognitive decline and dementia, and an early presentation of neurodegenerative diseases in some. Lastly, we will discuss future directions in the field so as to better understand the neurobiological basis of NPS in the early stages of the AD continuum, and their role in predicting AD pathophysiological progression and incident dementia.
Highlights
Neuropsychiatric symptoms (NPS) are non-cognitive symptoms common in the Alzheimer's disease (AD) continuum (Lyketsos et al, 2011; Brodaty et al, 2015; Vik-Mo et al, 2018), associated with poorer cognitive, functional, and quality of life outcomes, and accelerated progression to severe dementia (Teng et al, 2007; Karttunen et al, 2011; Fischer et al, 2012; Peters et al, 2015)
A larger study of 65 mild cognitive impairment (MCI) individuals from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database showed an AD-specific pattern of PCC hypometabolism in MCI subjects with apathy (Delrieu et al, 2014)
This was corroborated by a subsequent ADNI study including 422 cognitively normal, MCI, and early dementia subjects, demonstrating correlation between PCC hypometabolism and higher apathy scores (Gatchel et al, 2017)
Summary
Neuropsychiatric symptoms (NPS) are non-cognitive symptoms common in the Alzheimer's disease (AD) continuum (Lyketsos et al, 2011; Brodaty et al, 2015; Vik-Mo et al, 2018), associated with poorer cognitive, functional, and quality of life outcomes, and accelerated progression to severe dementia (Teng et al, 2007; Karttunen et al, 2011; Fischer et al, 2012; Peters et al, 2015). [18F]fluorodeoxyglucose ([18F]FDG) positron emission tomography (PET) measures cerebral glucose metabolic rate (CMRglc) changes and AD studies using [18F]FDG PET have demonstrated correlations between CMRglc reduction in the parietotemporal, posterior cingulate (PCC), and medial temporal and/or frontal cortices and synaptic dysfunction (Jack et al, 2016). Progressive CMRglc reductions occur years prior to clinical symptoms in patients with pathologically verified AD (Mosconi et al, 2009) and the degree of CMRglc reduction relates to disease severity (Furst et al, 2012). Studies in depression (Kennedy et al, 2001) and schizophrenia demonstrate regional cerebral metabolic dysfunction correlating with psychiatric symptoms.
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