Beyond Memory: A Focus on the Other Neuropsychiatric Symptoms of Dementia

Peters, Matthew E.

doi:10.1016/j.jagp.2014.11.002

Cited by 18 publications

(16 citation statements)

References 11 publications

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“…vascular depression. 40,41 Recent studies have reported inconsistent associations between NPS and AD pathology, [42][43][44] while providing some evidence for associations with non-AD biomarkers. 40,45,46 Our findings suggested substantial fluctuations over time with no coherent pattern of decline or increase in NPS as the disease progresses leaving room open for other factors affecting NPS in AD.…”

Section: Discussionmentioning

confidence: 99%

“… 39 Several theories have been proposed to explain the manifestation of NPS in AD. 3 , 40 While the symptom hypothesis states that NPS result from AD-related neuropathology that also contributes to cognitive impairment in AD, the risk factor hypothesis suggests that NPS arise from concurrent non-AD pathology, e.g., vascular depression. 40 , 41 Recent studies have reported inconsistent associations between NPS and AD pathology, 42 - 44 while providing some evidence for associations with non-AD biomarkers.…”

Section: Discussionmentioning

confidence: 99%

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Neuropsychiatric and Cognitive Symptoms Across the Alzheimer Disease Clinical Spectrum

et al. 2021

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Background and ObjectivesTo investigate the prevalence and trajectories of neuropsychiatric symptoms (NPS) in relation to cognitive functioning in a cohort of β-amyloid–positive (A+) individuals across the Alzheimer disease (AD) clinical spectrum.MethodsIn this single-center observational study, we included all individuals who visited the Alzheimer Center Amsterdam and had a clinical diagnosis of subjective cognitive decline (SCD), mild cognitive impairment (MCI), or probable AD dementia and were A+. We measured NPS with the Neuropsychiatric Inventory (NPI), examining total scores and the presence of specific NPI domains. Cognition was assessed across 5 cognitive domains and with the Mini-Mental State Examination (MMSE). We examined trajectories including model-based trends for NPS and cognitive functioning over time. We used linear mixed models to relate baseline NPI scores to cognitive functioning at baseline (whole-sample) and longitudinal time points (subsample n = 520, mean 1.8 [SD 0.7] years follow-up).ResultsWe included 1,524 A+ individuals from the Amsterdam Dementia Cohort with A+ SCD (n = 113), A+ MCI (n = 321), or A+ AD dementia (n = 1,090). NPS were prevalent across all clinical AD stages (≥1 NPS 81.4% in SCD, 81.2% in MCI, 88.7% in dementia; ≥1 clinically relevant NPS 54.0% in SCD, 50.5% in MCI, 66.0% in dementia). Cognitive functioning showed a uniform gradual decline; while in contrast, large intraindividual heterogeneity of NPS was observed over time across all AD groups. At baseline, we found associations between NPS and cognition in dementia that were most pronounced for NPI total scores and MMSE (range β = −0.18 to −0.11, false discovery rate [FDR]–adjusted p < 0.05), while there were no cross-sectional relationships in SCD and MCI (range β = −0.32 to 0.36, all FDR-adjusted p > 0.05). There were no associations between baseline NPS and cognitive functioning over time in any clinical stage (range β = −0.13 to 0.44, all FDR-adjusted p > 0.05).DiscussionNPS and cognitive symptoms are both prevalent across the AD clinical spectrum, but show a different evolution during the course of the disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neuropsychiatric and Cognitive Symptoms Across the Alzheimer Disease Clinical Spectrum

et al. 2021

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show abstract

Section: Discussionmentioning

confidence: 99%

“…40,41 Recent studies have reported inconsistent associations between NPS and AD pathology, 42-44 while providing some evidence for associations with non-AD biomarkers. 40, 45, 46 Our findings suggested substantial fluctuations over time with no coherent pattern of decline or increase in NPS as the disease progresses leaving room open for other factors affecting NPS in AD. In addition to neurobiological causes, a variety of psychosocial factors have been proposed to play a role in the emergence and worsening of NPS in AD including unmet needs, stress among caregivers, and environmental triggers.…”

Section: Discussionmentioning

confidence: 99%

Neuropsychiatric and cognitive symptoms across the Alzheimer’s disease clinical spectrum: Cross-sectional and longitudinal associations

Eikelboom

Berg

Singleton

et al. 2021

Preprint

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Objective: To investigate the prevalence and trajectories of neuropsychiatric symptoms (NPS) in relation to cognitive functioning in a cohort of amyloid-β positive individuals across the Alzheimer's disease (AD) clinical spectrum. Methods: We included 1,524 amyloid-β positive individuals from the Amsterdam Dementia Cohort with subjective cognitive decline (SCD, n=113), mild cognitive impairment (MCI, n=321), or dementia (n=1,090). We measured NPS with the neuropsychiatric inventory (NPI), examining total scores and the presence of specific NPI-items. Cognition was assessed across five cognitive domains and with the MMSE. We examined trajectories including model based trends for NPS and cognitive functioning over time. We used linear mixed models to relate baseline NPI scores to cognitive functioning at baseline (whole-sample) and longitudinal time-points (subsample n=520, Mean=1.8 [SD=0.7] years follow-up). Results: NPS were prevalent across all clinical AD stages (NPI total score ≥1 81.4% in SCD, 81.2% in MCI, 88.7% in dementia). Cognitive functioning showed an uniform gradual decline; while in contrast, large intra-individual heterogeneity of NPS was observed over time across all groups. At baseline, we found associations between NPS and cognition in dementia that were most pronounced for NPI total scores and MMSE (range β:-0.18—0.11, FDR-adjusted p<0.05), while there were no cross-sectional relationships in SCD and MCI (β:-0.32—0.36, FDR-adjusted p>0.05). There were no associations between baseline NPS and cognitive functioning over time in any clinical stage (β:-0.13—0.44, FDR-adjusted p>0.05). Conclusion: NPS and cognitive symptoms are both prevalent across the AD continuum, but show a different evolution during the course of the disease.

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“…Alternative, and possibly complementary, models propose that depressive symptoms may be causal factors accelerating AD progression or they may be stigmata of AD, even as early as ‘preclinical’ stages. (7) It is also possible that these roles may differ by symptom or symptom-clusters or across time and disease stages. Understanding these mechanisms is important to accurately classify and treat CN individuals at high risk for early AD progression and to differentiate these individuals from older adults with psychiatric symptoms distinct from AD-related processes.…”

Section: Introductionmentioning

confidence: 99%

Longitudinal Association of Amyloid Beta and Anxious-Depressive Symptoms in Cognitively Normal Older Adults

Donovan

Locascio

Marshall

et al. 2018

AJP

182

112

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Higher amyloid beta burden was associated with increasing anxious-depressive symptoms over time in cognitively normal older individuals. Prior depression history was related to higher but not worsening symptom ratings. These results suggest a direct or indirect association of elevated amyloid beta levels with worsening anxious-depressive symptoms and support the hypothesis that emerging neuropsychiatric symptoms represent an early manifestation of preclinical Alzheimer's disease.

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Beyond Memory: A Focus on the Other Neuropsychiatric Symptoms of Dementia

Cited by 18 publications

References 11 publications

Neuropsychiatric and Cognitive Symptoms Across the Alzheimer Disease Clinical Spectrum

Neuropsychiatric and Cognitive Symptoms Across the Alzheimer Disease Clinical Spectrum

Neuropsychiatric and cognitive symptoms across the Alzheimer’s disease clinical spectrum: Cross-sectional and longitudinal associations

Longitudinal Association of Amyloid Beta and Anxious-Depressive Symptoms in Cognitively Normal Older Adults

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