O2‐08‐05: Mild Behavioral Impairment: Prevalence in Clinical Setting and Cognitive Correlates

Cano, Jemellee; Chan, Victoria; Kan, Cheuk Ni; Chen, Christopher; Hilal, Saima; Venketasubramanian, Narayanaswamy; Xu, Xin

doi:10.1016/j.jalz.2018.06.2685

Cited by 8 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This analysis was conducted in the subset of participants with normal cognition at year 1 and year 2 (the timeline of this analysis is further depicted in Additional file 2)-those who reported anxiety or SCD at both years were deemed as having "consistent" symptoms, while those who reported anxiety or SCD at either year only were deemed as having "inconsistent" symptoms. The use of two consecutive annual visits (year 1 and year 2) to determine symptom consistency is not inconsistent with what has been done in the literature [35][36][37]. In particular, "consistent" SCD has also been shown to be more predictive of neurocognitive disorders in recent literature [35,38,39].…”

Section: Statistical Analysesmentioning

confidence: 88%

Subjective cognitive decline, anxiety symptoms, and the risk of mild cognitive impairment and dementia

Liew

2020

Alz Res Therapy

View full text Add to dashboard Cite

Background Subjective cognitive decline (SCD) and anxiety symptoms both predict neurocognitive disorders, but the two correlate strongly with each other. It is unclear whether they reflect two independent disease processes in the development of neurocognitive disorders and hence deserve separate attention. This cohort study examined whether SCD and anxiety symptoms demonstrate independent risks of mild cognitive disorder and dementia (MCI/dementia). Methods The study included 14,066 participants aged ≥ 50 years and diagnosed with normal cognition at baseline, recruited from Alzheimer’s Disease Centers across the USA. The participants were evaluated for SCD and anxiety symptoms at baseline and followed up almost annually for incident MCI/dementia (median follow-up 4.5 years; interquartile range 2.2–7.7 years). SCD and anxiety symptoms were included in Cox regression to investigate their independent risks of MCI/dementia. Results SCD and anxiety symptoms demonstrated independent risks of MCI/dementia, with HR 1.9 (95% CI 1.7–2.1) and 1.3 (95% CI 1.2–1.5), respectively. Co-occurring SCD and anxiety symptoms demonstrated the highest risk (HR 2.4, 95% CI 1.9–2.9)—participants in this group had a 25% probability of developing MCI/dementia by 3.1 years (95% 2.4–3.7), compared to 8.2 years among those without SCD or anxiety (95% CI 7.9–8.6). The results remained robust even in the sensitivity analyses that took into account symptom severity and consistency of symptoms in the first 2 annual visits. Conclusions The findings suggest that clinicians should not dismiss one over the other when patients present with both SCD and anxiety and that both constructs may potentially be useful to identify high-risk populations for preventive interventions and trials. The findings also point to the need for further research to clarify on the neurobiological distinctions between SCD and anxiety symptoms, which may potentially enrich our understanding on the pathogenesis of neurocognitive disorders.

show abstract

Section: Statistical Analysesmentioning

confidence: 88%

Subjective cognitive decline, anxiety symptoms, and the risk of mild cognitive impairment and dementia

Liew

2020

Alz Res Therapy

View full text Add to dashboard Cite

show abstract

“…Thus far, clinical and imaging/biomarker studies have validated MBI as a risk state and marker of early disease. Cross-sectional studies have associated MBI with a specific cognitive profile in pre-dementia [28] and Parkinson's disease [29], and longitudinal data have demonstrated faster cognitive decline in the presence of MBI [12,28,30,31]. Neurobiological correlates of MBI are also emerging.…”

Section: Discussionmentioning

confidence: 99%

Plasma Neurofilament Light: A Marker of Neurodegeneration in Mild Behavioral Impairment

Naude

Gill

et al. 2020

JAD

View full text Add to dashboard Cite

Background: Assessing neuropsychiatric symptoms (NPS) in older adults is important for determining dementia risk. Mild behavioral impairment (MBI) is an at-risk state for cognitive decline and dementia, characterized by emergent NPS in later life. MBI has significantly higher dementia incidence than late life psychiatric conditions. However, its utility as a proxy for neurodegeneration has not been demonstrated. Plasma neurofilament light (NfL) is a validated biomarker of axonal damage, and has been shown to associate with hallmarks of neurodegeneration. Objective: The purpose of this investigation was to identify associations between NfL rate of change and the presence of MBI symptomatology. Methods: We evaluated the association of MBI with changes in NfL in a cohort (n = 584; MBI + n = 190, MBIn = 394) of non-demented participants from the Alzheimer's Disease Neuroimaging Initiative. MBI was determined by transforming Neuropsychiatric Inventory Questionnaire items using a published algorithm. Change in NfL was calculated over 2 years. Results: Time*MBI status was the only significant interaction to predict change in NfL concentrations (F(1,574) = 4.59, p = 0.032), even after controlling for age, mild cognitive impairment, and demographics. Analyses reclassifying 64 participants with new onset MBI over 2 years similarly demonstrated greater increases in NfL (F(1,574) = 5.82, p = 0.016).

show abstract

“…MBI is a validated construct, separate from psychiatric illness, demonstrating a significantly higher 5‐year progression rate to dementia than late life psychiatric disorders (Taragano et al, ). Further, in those with no cognitive impairment or MCI, the presence of MBI is associated with a significantly higher 3‐year progression to dementia than those without MBI (Cano et al, ). As described in the MBI criteria, and operationalized in the MBI checklist (MBI‐C, developed explicitly as a case ascertainment instrument for MBI [Ismail et al, ]), the NPS components of MBI have been clustered into the following domains: decreased motivation, affective dysregulation, impulse dyscontrol, social inappropriateness, and abnormal perception/thought content.…”

Section: Methodsmentioning

confidence: 99%

Association of Alzheimer's genetic loci with mild behavioral impairment

Andrews

Ismail

Anstey

et al. 2018

American J of Med Genetics Pt B

View full text Add to dashboard Cite

Mild behavioral impairment (MBI) describes the emergence of later-life neuropsychiatric symptoms (NPS) as an at-risk state for incident cognitive decline and dementia, and for some as a potential manifestation of prodromal dementia. How NPS mechanistically link to the development of mild cognitive impairment and Alzheimer's disease (AD) is not fully understood, with potential mechanisms including shared risk factors related to both NPS and cognitive impairment, or AD pathology promoting NPS. This is the first exploratory study to examine whether AD genetic loci as a genetic risk score (GRS), or individually, are a shared risk factor with MBI. Participants were 1,226 older adults (aged 72-79; 738 males; 763 normal cognition) from the Personality and Total Health Through Life project. MBI was approximated in accordance with Criterion 1 of the ISTAART-AA diagnostic criteria using a transformation algorithm for the neuropsychiatric inventory. A GRS was constructed from 25 AD risk loci. Binomial logistic regression adjusting for age, gender, and education examined the association between GRS and MBI. A higher GRS and APOE*ε4 were associated with increased likelihood of affective dysregulation. Nominally significant associations were observed between MS4A4A-rs4938933*C and MS4A6A-rs610932*G with a reduced likelihood of affective dysregulation; ZCWPW1-rs1476679*C with a reduced likelihood of social inappropriateness and abnormal perception/thought content; BIN1-rs744373*G and EPHA1-rs11767557*C with higher likelihood of abnormal perception/thought content; NME8-rs2718058*G with a reduced likelihood of decreased motivation. These preliminary findings suggest a common genetic etiology between MBI and traditionally recognized cognitive problems observed in AD and improve our understanding of the pathophysiological features underlying MBI. K E Y W O R D SAlzheimer's disease, genetic risk score, MBI

show abstract

O2‐08‐05: Mild Behavioral Impairment: Prevalence in Clinical Setting and Cognitive Correlates

Cited by 8 publications

References 0 publications

Subjective cognitive decline, anxiety symptoms, and the risk of mild cognitive impairment and dementia

Subjective cognitive decline, anxiety symptoms, and the risk of mild cognitive impairment and dementia

Plasma Neurofilament Light: A Marker of Neurodegeneration in Mild Behavioral Impairment

Association of Alzheimer's genetic loci with mild behavioral impairment

Contact Info

Product

Resources

About