Prevalence of Neuropsychiatric Symptoms in Dementia and Mild Cognitive Impairment

Lyketsos, Constantine G.; López, Oscar L.; Jones, Beverly N.; Fitzpatrick, Annette L.; Breitner, John C.S.; DeKosky, Steven T.

doi:10.1001/jama.288.12.1475

Cited by 1,845 publications

(1,628 citation statements)

References 62 publications

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“…Thirty-one percent of participants with CIND had at least one NPS, a rate halfway between that in the cognitively normal (15%) and those with dementia (60%). These rates are comparable to those reported in the Cardiovascular Health Study 11 and by Geda et al 12 . A subgroup analysis comparing participants with aMCI to those with other types of CIND showed no significant differences.…”

Section: Objectivesupporting

confidence: 89%

“…If this was endorsed, specific follow up questions were asked to clarify the nature of the symptoms, and their frequency, severity, degree of change from premorbid, and treatment. As in previous studies 11, 12 , the NPS outcome variable was defined as either the presence or absence of a given NPS domain. The NPI was also analyzed by dividing into absence of any NPS versus ≥1 NPS (NPI Total).…”

Section: Methodsmentioning

confidence: 99%

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Neuropsychiatric Symptoms as Risk Factors for Progression From CIND to Dementia: The Cache County Study

Peters¹,

Rosenberg²,

Steinberg³

et al. 2013

The American Journal of Geriatric Psychiatry

133

104

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Objectives To examine the association of neuropsychiatric symptom (NPS) severity with risk of transition to all-cause dementia, Alzheimer's disease (AD), and vascular dementia (VaD). Design Survival analysis of time to dementia, AD, or VaD onset. Setting Population-based study. Participants 230 participants diagnosed with cognitive impairment, no dementia (CIND) from the Cache County Study of Memory Health and Aging were followed for a mean of 3.3 years. Measurements The Neuropsychiatric Inventory (NPI) was used to quantify the presence, frequency, and severity of NPS. Chi-square statistics, t-tests, and Cox proportional hazard ratios were used to assess associations. Results The conversion rate from CIND to all-cause dementia was 12% per year, with risk factors including an APOE ε4 allele, lower MMSE, lower 3MS, and higher CDR sum-of-boxes. The presence of at least one NPS was a risk factor for all-cause dementia, as was the presence of NPS with mild severity. Nighttime behaviors were a risk factor for all-cause dementia and of AD, while hallucinations were a risk factor for VaD. Conclusions These data confirm that NPS are risk factors for conversion from CIND to dementia. Of special interest is that even NPS of mild severity are a risk for all-cause dementia or AD.

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Section: Objectivesupporting

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Neuropsychiatric Symptoms as Risk Factors for Progression From CIND to Dementia: The Cache County Study

Peters¹,

Rosenberg²,

Steinberg³

et al. 2013

The American Journal of Geriatric Psychiatry

133

104

View full text Add to dashboard Cite

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“…Cognitive impairment that does not reach the threshold for dementia diagnosis is not only associated with increased risk for progression to dementia (Fratiglioni and Qiu, 2011;Petersen, 2004;Winblad et al, 2004), but also increased health care costs (Albert et al, 2002), increased neuropsychiatric symptoms (Lyketsos et al, 2002), and increased functional disability (McGuire et al, 2006). Age-related decline in episodic memory, attention, and executive function is reported in both longitudinal (Meijer et al, 2009;Tucker-Drob et al, 2009) and cross-sectional studies (Coubard et al, 2011;Kray and Lindenberger, 2000).…”

Section: Introductionmentioning

confidence: 99%

The impact of cognitive training and mental stimulation on cognitive and everyday functioning of healthy older adults: A systematic review and meta-analysis

Kelly

Loughrey

Lawlor

et al. 2014

Ageing Research Reviews

403

291

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“…Alzheimer's disease (AD) is characterized by progressive impairment of memory accompanied by psychiatric disturbances (Lyketsos et al, 2002;Petersen, 2004). Behavioral abnormalities in AD result from dysfunction and death of neurons in brain regions involved in cognition and mood such as the hippocampus, amygdala and associated cortical regions.…”

Section: Introductionmentioning

confidence: 99%

Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice

Nelson

Guo

Halagappa

et al. 2007

Experimental Neurology

163

133

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A history of depression is a risk factor for Alzheimer's disease (AD), suggesting the possibility that antidepressants administered prophylactically might retard the disease process and preserve cognitive function. Here we report that pre-symptomatic treatment with the antidepressant paroxetine attenuates the disease process and improves cognitive performance in the 3xTgAD mouse model of AD. Five month-old male and female 3xTgAD and non-transgenic mice were administered either paroxetine or saline daily for 5 months. Open-field activity was tested in 7 month-old mice and performance in passive avoidance and Morris swim tasks were evaluated at 10 months. 3xTgAD mice exhibited reduced exploratory activity, increased transfer latency in the passive avoidance test and impaired performance in the Morris spatial navigation task compared to nontransgenic control mice. Paroxetine treatment ameliorated the spatial navigation deficit in 3xTgAD male and female mice, without affecting swim speed or distance traveled, suggesting a preservation of cognitive function. Levels of amyloid beta-peptide (Aβ) and numbers of Aβ immunoreactive neurons were significantly reduced in the hippocampus of male and female paroxetine-treated 3xTgAD mice compared to saline-treated 3xTgAD mice. Female 3xTgAD mice exhibited significantly less tau pathology in the hippocampus and amygdala compared to male 3xTgAD mice, and paroxetine lessened tau pathology in male 3xTgAD mice. The ability of a safe and effective antidepressant to suppress neuropathological changes and improve cognitive performance in a mouse model, suggests that such drugs administered prophylactically might retard the development of AD in humans.

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Prevalence of Neuropsychiatric Symptoms in Dementia and Mild Cognitive Impairment

Cited by 1,845 publications

References 62 publications

Neuropsychiatric Symptoms as Risk Factors for Progression From CIND to Dementia: The Cache County Study

Neuropsychiatric Symptoms as Risk Factors for Progression From CIND to Dementia: The Cache County Study

The impact of cognitive training and mental stimulation on cognitive and everyday functioning of healthy older adults: A systematic review and meta-analysis

Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice

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