Mini-Mental State Examination Decline Research Articles

Longitudinal assessment of plasma biomarkers for early detection of cognitive changes in subjective cognitive decline

BackgroundIndividuals experiencing subjective cognitive decline (SCD) are at an increased risk of developing mild cognitive impairment and dementia. Early identification of SCD and neurodegenerative diseases using biomarkers may help clinical decision-making and improve prognosis. However, few cross-sectional and longitudinal studies have explored plasma biomarkers in individuals with SCD using immunomagnetic reduction.ObjectiveTo identify plasma biomarkers for SCD.MethodsFifty-two participants [38 with SCD, 14 healthy controls (HCs)] underwent baseline assessments, including measurements of plasma Aβ42, Aβ40, t-tau, p-tau, and α-synuclein using immunomagnetic reduction (IMR) assays, cognitive tests and the Mini-Mental State Examination (MMSE). Following initial cross-sectional analysis, 39 individuals (29 with SCD, 10 HCs) entered a longitudinal phase for reassessment of these biomarkers and the MMSE. Biomarker outcomes across different individual categories were primarily assessed using the area under the receiver operating characteristic (ROC) curve. The SCD subgroup with an MMSE decline over one point was compared to those without such a decline.ResultsHigher baseline plasma Aβ1-42 levels significantly discriminated participants with SCD from HCs, with an acceptable area under the ROC curve (AUC) of 67.5% [95% confidence interval (CI), 52.7–80.0%]. However, follow-up and changes in MMSE and IMR data did not significantly differ between the SCD and HC groups (p > 0.05). Furthermore, lower baseline plasma Aβ1-42 levels were able to discriminate SCD subgroups with and without cognitive decline with a satisfied performance (AUC, 75.0%; 95% CI, 55.6–89.1%). At last, the changes in t-tau and Aβ42 × t-tau could differentiate between the two SCD subgroups (p < 0.05).ConclusionBaseline plasma Aβ42 may help identify people with SCD and predict SCD progression. The role of plasma Aβ42 levels as well as their upward trends from baseline in cases of SCD that progress to mild cognitive impairment and Alzheimer’s disease require further investigation.

Clinical value of plasma ALZpath pTau217 immunoassay for assessing mild cognitive impairment

BackgroundAmong plasma biomarkers for Alzheimer’s disease (AD), pTau181 and pTau217 are the most promising. However, transition from research to routine clinical use will require confirmation of clinical performance in prospective...

APOE-ε4 alleles modify the decline of MMSE scores associated with time-dependent PM2.5 exposure: Findings from a Community-based Longitudinal Cohort Study

Background: Limited research has explored the long-term effect of reduced PM2.5 exposure on cognitive function. This study aimed to investigate the effects of time-dependent PM2.5 exposure and the interactions of PM2.5 and aging on declines in Mini-Mental State Examination (MMSE) scores, in carriers and non-carriers of the APOE-ε4 allele. Methods: Participants aged over 60 were recruited for this cohort study, undergoing MMSE tests twice from the Taiwan Biobank Program from 2008 to 2020. Participants with dementia or baseline MMSE scores < 24 were excluded. Annual PM2.5 levels were estimated using a hybrid kriging/land use regression model with extreme gradient boosting, treated as a time-dependent variable. Generalized estimating equations were used to assess the impacts of repeated PM2.5 on MMSE decline, further stratified by the presence of APOE-ε4 alleles. Results: After follow-up, 290 participants out of the overall 7,000 community residents in the Biobank dataset demonstrated incidences of MMSE declines (< 24), with an average MMSE score decline of 1.11 per year. Participants with ε4/ε4 alleles in the APOE gene had significantly 3.68-fold risks of MMSE decline. High levels of PM2.5 across all visits were significantly associated with worsening of scores on the overall MMSE. As annual levels of PM2.5 decreased over time, the impact of PM2.5 on MMSE decline also slowly diminished. Conclusion: Long-term PM2.5 exposure may be associated with increased risk of MMSE decline, despite improvements in ambient PM2.5 levels over time. Validation of these results necessitates a large-scale prospective cohort study with more concise cognitive screening tools.

Head-to-head comparison between plasma p-tau217 and flortaucipir-PET in amyloid-positive patients with cognitive impairment

BackgroundPlasma phosphorylated tau (p-tau) has emerged as a promising biomarker for Alzheimer’s disease (AD). Studies have reported strong associations between p-tau and tau-PET that are mainly driven by differences between amyloid-positive and amyloid-negative patients. However, the relationship between p-tau and tau-PET is less characterized within cognitively impaired patients with a biomarker-supported diagnosis of AD. We conducted a head-to-head comparison between plasma p-tau217 and tau-PET in patients at the clinical stage of AD and further assessed their relationships with demographic, clinical, and biomarker variables.MethodsWe retrospectively included 87 amyloid-positive patients diagnosed with MCI or dementia due to AD who underwent structural MRI, amyloid-PET (11C-PIB), tau-PET (18F-flortaucipir, FTP), and blood draw assessments within 1 year (age = 66 ± 10, 48% female). Amyloid-PET was quantified in Centiloids (CL) while cortical tau-PET binding was measured using standardized uptake value ratios (SUVRs) referenced against inferior cerebellar cortex. Plasma p-tau217 concentrations were measured using an electrochemiluminescence-based assay on the Meso Scale Discovery platform. MRI-derived cortical volume was quantified with FreeSurfer. Mini-Mental State Examination (MMSE) scores were available at baseline (n = 85) and follow-up visits (n = 28; 1.5 ± 0.7 years).ResultsPlasma p-tau217 and cortical FTP-SUVR were correlated (r = 0.61, p < .001), especially in temporo-parietal and dorsolateral frontal cortices. Both higher p-tau217 and FTP-SUVR values were associated with younger age, female sex, and lower cortical volume, but not with APOE-ε4 carriership. PIB-PET Centiloids were weakly correlated with FTP-SUVR (r = 0.26, p = 0.02), but not with p-tau217 (r = 0.10, p = 0.36). Regional PET-plasma associations varied with amyloid burden, with p-tau217 being more strongly associated with tau-PET in temporal cortex among patients with moderate amyloid-PET burden, and with tau-PET in primary cortices among patients with high amyloid-PET burden. Higher p-tau217 and FTP-SUVR values were independently associated with lower MMSE scores cross-sectionally, while only baseline FTP-SUVR predicted longitudinal MMSE decline when both biomarkers were included in the same model.ConclusionPlasma p-tau217 and tau-PET are strongly correlated in amyloid-PET-positive patients with MCI or dementia due to AD, and they exhibited comparable patterns of associations with demographic variables and with markers of downstream neurodegeneration.

Association between neighborhood availability of physical activity facilities and cognitive performance in older adults

The existing evidence on the contextual influence of the availability of local facilities for physical activity on the cognitive health of elderly residents is sparse. This study examined the association between neighborhood physical activity facilities and cognitive health in older individuals. A cohort study of community-dwelling older adults was performed using baseline data and follow-up data from the Taiwan Biobank. Cognitive health was measured in 32,396 individuals aged 60–70 years using the Mini-Mental State Examination (MMSE) with follow-up information on 8025 participants. The district was used as the proxy for local neighborhood. To determine neighborhood physical activity facilities, school campuses, parks, activity centers, gyms, swimming pools, and stadiums were included. Multilevel linear regression models were applied to examine the associations of neighborhood physical activity facilities with baseline MMSE and MMSE decline during follow-up, with adjustment for individual factors and neighborhood socioeconomic characteristics. Multilevel analyses revealed that there was a neighborhood-level effect on cognitive health among older adults. After adjusting for compositional and neighborhood socioeconomic characteristics, baseline MMSE was higher in individuals living in the middle- (beta = 0.12, p-value = 0.140) and high-density facility (beta = 0.22, p-value = 0.025) groups than in the low-density group (p-value for trend-test = 0.031). MMSE decline during follow-up was slower in the middle- (beta = 0.15, p-value = 0.114) and high-density facility (beta = 0.27, p-value = 0.052) groups than in the low-density group (p-value for trend-test = 0.032). Greater neighborhood availability of physical activity facilities was associated with better cognitive health among older residents. These findings have implications for designing communities and developing strategies to support cognitive health of an aging population.

Social interaction level modulates the impact of frailty on cognitive decline: a longitudinal study

Objectives This study evaluates whether social interaction level modifies the association between frailty and cognitive decline in older adults. Methods A total of 2701 adults aged ≥65 years enrolled in the Progetto Veneto Anziani (Pro.V.A.), participated in the study. At baseline, participants were classified as having low, moderate, or high social interactions based on: cohabiting status, frequency of contacts with relatives/friends or involvement in childcare activities, and frequency of participation in social or community activities. Baseline frailty was defined as the presence of ≥3 criteria among: weight loss, weakness, slowness, low physical activity, and exhaustion. Cognitive function was assessed through the Mini-Mental State Examination (MMSE) at baseline and after 4.4 and 7 years. The association between frailty and MMSE changes over time was evaluated through linear mixed models. Interaction and subgroup analyses explored the modifying effect of social interaction level on the above association. Results The mean age of participants was 76.1 years, and 59.1% were women. Frail individuals had a steeper annual MMSE decline than their non-frail counterparts (ß=-0.40, 95%CI: −0.59, −0.20). When stratifying participants by social interaction level, we found that the association between frailty and MMSE changes over time was stronger in those with low social interactions (ß=-0.74, 95%CI: −1.33, −0.15) while attenuated in those with moderate (ß=-0.42, 95%CI: −0.74, −0.11) or high social interaction level (ß=-0.29, 95%CI: −0.58, 0.01). Conclusion Maintaining frequent social interactions might mitigate the negative impact of frailty on older people’s cognitive functions.

Methylation status and sulfur amino-acids as risk factors for cognitive decline over 12 years: A longitudinal population based study (P4-6.002)

<h3>Objective:</h3> To investigate the association of vitamin B12, folate, and sulfur amino-acids with cognitive decline in a large sample of community dwelling older adults. <h3>Background:</h3> Impairment of methylation status and raised values of homocysteine and cysteine are common conditions in older adults and may be modifiable risk factors for cognitive decline. <h3>Design/Methods:</h3> From the Swedish National Study of Aging and Care in Kungsholmen (SNAC-K), 2900 dementia-free individuals at baseline aged 60–102 years with comprehensive assessments and Mini-mental state examination (MMSE) were recruited. A total of 2202 participants underwent repeated MMSE assessments up to 5 occasions over 12 years. The association of baseline vitamin B12, holotranscobalamin, folate, homocysteine, methionine, cystathionine, cysteine, glutathione, and methylation status (defined as serum methionine/homocysteine ratio) with rate of cognitive decline was examined using linear mixed models, adjusted for several potential confounders, including common vascular risk factors. <h3>Results:</h3> After adjusting for age, sex, education, creatinine, albumin, smoking status, systolic blood pressure, and <i>APOE</i>ɛ4 status, raised baseline serum total homocysteine and cysteine values were associated with a faster rate of cognitive decline: for the highest quartile compared with the lowest, β coefficient and standard error (SE) were −0.0058 (0.002) for homocysteine (p=0.004) and −0.0051 (0.002) for cysteine (p=0.014). In contrast, a better methylation status was associated with less MMSE decline over 15 years: β (SE) was 0.0058 (0.002) for the highest quartile compared with the lowest (p=0.004). Furthermore, elevated methionine values tended to slow rate of cognitive decline (p=0.079). No relationships were found for other sulfur amino acids, vitamin B12 or folate. <h3>Conclusions:</h3> Markers of methylation status and raised cysteine values were related to more rapid cognitive decline over 12 years, suggesting that optimizing homocysteine, cysteine, and methionine values may be important in reducing the risk of cognitive decline in older adults. <b>Disclosure:</b> Babak Hooshmand has nothing to disclose.

Obstructive sleep apnoea and 5-year cognitive decline in the elderly.

The relationship between obstructive sleep apnoea (OSA) and cognitive decline remains controversial, especially in the elderly population. We used data from the HypnoLaus study to assess associations between OSA and longitudinal cognitive changes in a sample of community-dwelling elderly individuals. We studied associations between polysomnographic OSA parameters (of breathing/hypoxaemia and sleep fragmentation) and cognitive changes over a 5-year period, after adjustment for potential confounders. The primary outcome was the annual change in cognitive scores. The moderating effects of age, sex and apolipoprotein E4 (ApoE4) status were also examined. 358 elderly individuals without dementia were included (mean±sd age 71.0±4.2 years; 42.5% males). A lower mean peripheral oxygen saturation (S pO2 ) during sleep was associated with a steeper decline in Mini-Mental State Examination (B= -0.12, p=0.004), Stroop test condition 1 (B=0.53, p=0.002) and Free and Cued Selective Reminding Test delayed free recall (B= -0.05, p=0.008). A longer time spent asleep with S pO2 <90% was associated with a steeper decline in Stroop test condition 1 (B=0.47, p=0.006). Moderation analysis showed that apnoea-hypopnoea index and oxygen desaturation index were associated with a steeper decline in global cognitive function, processing speed and executive function only in older participants, men and ApoE4 carriers. Our results provide evidence of the contribution of OSA and nocturnal hypoxaemia to cognitive decline in the elderly population.

Cognitive Function Deterioration After Cardiopulmonary Bypass: Can Intraoperative Optimal Cerebral Regional Tissue Oxygen Saturation Predict Postoperative Cognitive Function?

Cognitive impairment is a common neurologic complication after cardiac surgery with cardiopulmonary bypass (CPB). This study evaluated postoperative cognitive function to determine predictors of cognitive dysfunction, including intraoperative cerebral regional tissue oxygen saturation (rSO2). A prospective observational cohort study. At a single academic tertiary-care center. A total of 60 adults undergoing cardiac surgery with CPB from January to August 2021. None. All patients underwent Mini-Mental State Examination (MMSE) and quantified electroencephalography (qEEG) 1 day before cardiac surgery, 7 days postoperatively (POD7), and POD60. Intraoperative cerebral rSO2 was monitored continuously. For MMSE, no significant decrease in MMSE score was found on POD7 versus preoperatively (p=0.09), but POD60 scores showed significant improvement compared with both preoperative (p=0.02) and POD7 scores (p < 0.001). On qEEG, relative theta power on POD7 was increased versus preoperatively (p < 0.001), but it was decreased on POD60 (POD7 versus POD60, p < 0.001), and was close to preoperative data (p > 0.99). Baseline rSO2 was an independent factor for postoperative MMSE. Both baseline and mean rSO2 showed a significant influence in postoperative relative theta activity, whereas mean rSO2 was the only predictor for the theta-gamma ratio (p=0.04). The MMSE in patients undergoing CPB declined at POD7 and recovered by POD60. Lower baseline rSO2 indicated a higher potential for MMSE decline at POD60. Inferior intraoperative mean rSO2 was related to higher postoperative relative theta activity and theta-gamma ratio, implying subclinical or further cognitive impairment.

IL-33/ST2 mediating systemic inflammation and neuroinflammation through NF-kB participated in the neurocognitive impairment in obstructive sleep apnea.

Increasing evidence has noted that neuroinflammation contributes to the pathological processes of cognitive impairment of obstructive sleep apnea (OSA) patients. Interleukin (IL) -33/suppression of tumorigenicity 2 (ST2) signaling pathway plays well-defined roles in the inflammatory progression. The study aims to elucidate whether IL-33/ST2 signaling pathway plays a role in the cognitive dysfunction in patients with OSA via regulating neuroinflammation. We found that compared with control subjects, patients with OSA showed significantly elevated IL-33, ST2 and p65 nuclear factor-kappa B (NF-κB) levels in peripheral blood mononuclear cells (PBMCs) and inflammatory cytokines IL-6, IL-8 in serum, which were positively correlated with disease severity. Meanwhile, OSA patients exhibited a decline in Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores, suggesting mild cognitive impairment. Continuous positive airway pressure (CPAP) treatment for 12weeks significantly decreased the expression of IL-33, ST2, p65NF-κB, IL-6 and IL-8, as well as improved cognitive function of OSA patients. Moreover, the IL-33/ST2 signaling was closely correlated with sleep respiratory parameters and cognitive dysfunction. To further explore the underlying mechanism of IL-33/ST2 signaling pathway, we stimulated human microglial clone 3 (HMC3) cells with lipopolysaccharide (LPS) to mimic neuroinflammatory response in vitro. The results showed that LPS treatment led to an increase in IL-33 and ST2 expression in a dose- dependent manner, along with an increased secretion of IL-6 and IL-8. Functional experiments showed that knockdown of IL-33 ameliorated LPS-induced neuroinflammation via suppressing NF-κB signaling. Overall, current findings suggest that IL-33/ST2 signaling participated in the cognitive impairment of OSA patients by promoting neuroinflammation via activating NF-κB signaling. These results may provide a novel therapeutic target for treating OSA- associated cognitive dysfunction.

Amyloid‐ß aggregation, APOE‐e genotype, and the trajectory of cognitive decline in persons without dementia

AbstractBackgroundThe association of amyloid abnormality with cognitive decline in persons with normal cognition (NC) and mild cognitive impairment (MCI) is important to guide AD trial design and understand prognoses. We examined the relation between amyloid abnormality and decline over time in several cognitive domains, and tested whether apolipoprotein (APOE)‐e genotype modified this association.MethodWe included 3,820 persons (2,599 NC, 1,221 all‐cause MCI) from 22 Amyloid Biomarker Study cohorts, with baseline PET (n = 846) or CSF (n = 2,974) amyloid measurements available. Amyloid abnormality on PET was based on visual read or cohort‐specific cutoffs, and for CSF on cohort‐specific or data‐driven cutoffs. Global cognition was assessed by Mini‐Mental State Examination (MMSE), functional performance by Clinical Dementia Rating global scale (CDR), and memory immediate and delayed recall by verbal learning tests. We examined baseline amyloid abnormality associations with cognitive performance over time and potential modification by APOE‐e (up to 3‐way interactions) using random‐slope/random‐intercept linear mixed‐models corrected for age, sex, education with random cohort effects.ResultMean follow‐up duration was 2.1 (range 0.5‐8) years. Baseline MMSE was worse in persons with abnormal‐amyloid compared with normal‐amyloid (NC mean difference = 0.2, p = 0.04, MCI mean difference = 2.4, p&lt;0.001). In NC, amyloid abnormality was not associated with decline in any domain (Table 1), nor was the association influenced by APOE‐e4. In MCI, amyloid abnormality was associated with lower baseline performance and steeper decline on all domains (Table 1). In APOE‐e4‐carriers with MCI, MMSE decline was steeper than in non‐carriers (p&lt;0.001, 1.5x steeper in amyloid‐abnormal, 3x steeper in amyloid‐normal). The rate of decline on immediate/delayed recall in MCI was higher in APOE‐e4‐carriers than non‐carriers, independent of amyloid status (p&lt;0.001). For both NC and MCI, decline was steepest in persons with e4e4, followed by e3e4, e3e3, e2e4, and e2e3 (p = 0.001, Figure 1), independent of amyloid status.ConclusionAmyloid abnormality was not associated with cognitive decline in persons with NC after a short‐term follow‐up. In MCI, amyloid abnormality was closely associated with cognitive decline in several domains, with an additive effect of APOE‐e on decline. These results may be relevant for future trial recruitment strategies. Future studies should examine long‐term outcomes in NC.

Association between Subclinical Epileptiform Discharge and the Severity of Cognitive Decline in Alzheimer's Disease: A Longitudinal Cohort Study.

Alzheimer's disease (AD) is the most common type of dementia. Aging is a risk factor for both AD and seizures. Subclinical epileptiform discharge (SED) has no evident clinical manifestation in patients with AD. Therefore, SED is liable to be overlooked in these patients since electroencephalography is not routinely performed in clinical settings. Previous studies about the association between SED and AD have yielded inconsistent results. The current study aimed to evaluate the prevalence of SED and its effect on AD severity and clinical outcomes. Patients with AD from Kaohsiung Municipal Ta-tung Hospital were included in this study. International 10-20 system scalp electroencephalography for 13 minutes was performed to detect SED. Clinical outcomes of patients with and without SED were assessed by neuropsychological tests [Cognitive Abilities Screening Instrument (CASI), Mini-Mental State Examination (MMSE), and Clinical Dementia Rating Scale Sum of Boxes (CDR-SOB)]. 288 patients (mean age 80.5 years, 60.4% female) were enrolled in this study. Fifty-seven (19.8%) out of 288 patients with AD had SED. The prevalence of SED increased with the severity of cognitive impairment. Compared with patients without SED, those with SED showed significantly greater decline in CASI (-9.32 versus -3.52 points, p = 0.0001) and MMSE (-2.52 versus -1.12 points, p = 0.0042) scores in one year. SED may play a significant role in AD progression and is a potential therapeutic target.

Trajectories of cognitive and physical performance after accidental falls in nursing home residents: A prospective study

This prospective study evaluated cognitive and physical trajectories of nursing home (NH) residents after fall occurrence and their predictors. In 167 residents aged ≥60, we considered the closest pre-fall assessment and up to the first three post-fall assessments of cognitive and physical functions performed through Mini-Mental State Examination (MMSE) and Tinetti tests. Mixture models identified three post-fall cognitive and physical trajectories: stability, slow decline, and rapid decline. At logistic regression, older age, fewer informal visits, and falls within one month from institutionalization increased the probability of experiencing a decline in MMSE and Tinetti scores. Worse pre-fall cognitive function increased the likelihood of cognitive and physical decline, while worse pre-fall Tinetti score negatively impacted only physical decline.In conclusion, the impact of falls on the cognitive and physical health of NH residents may be modulated by their pre-fall cognitive function and some modifiable factors, such as social interactions and physical function.

Blood Th17 cells and IL-17A as candidate biomarkers estimating the progression of cognitive impairment in stroke patients.

BackgroundT helper (Th) cells regulate immunity and inflammation to engage in cognitive impairment in several neurological diseases, while their clinical relevance in stroke patients is not clear. The current study intended to assess the relationship of Th1 cells, Th17 cells, interferon‐gamma (IFN‐γ), and interleukin (IL)‐17A with cognitive function in stroke patients.MethodsOne hundred twenty stroke patients and 40 controls were enrolled in this muticenter study. Th1 and Th17 cells in peripheral blood were assessed by flow cytometry; meanwhile, IFN‐γ and IL‐17A in serum were detected by enzyme‐linked immunosorbent assay. Cognitive function of stroke patients was evaluated by Mini‐Mental State Examination (MMSE) score at enrollment (baseline), year 1, year 2, and year 3.ResultsTh1 cells (p = 0.037) and IFN‐γ (p = 0.048) were slightly increased, while Th17 cells (p < 0.001) and IL‐17A (p < 0.001) were greatly elevated in stroke patients compared with controls. Th17 cells (r s = −0.374, p < 0.001) and IL‐17A (r s = −0.267, p = 0.003) were negatively correlated with MMSE score at baseline, but Th1 cells and IFN‐γ were not. Meanwhile, Th17 cells (p = 0.001) and IL‐17A (p = 0.024) were increased in patients with cognitive impairment compared to those without cognitive impairment. Notably, Th17 cells were positively associated with 1‐year (r s = 0.331, p < 0.001), 2‐year (r s = 0.261, p = 0.006), and 3‐year (r s = 0.256, p = 0.011) MMSE decline; IL‐17A was positively correlated with 1‐year (r s = 0.262, p = 0.005), 2‐year (r s = 0.193, p = 0.045), but not 3‐year MMSE decline. However, both Th1 cells and IFN‐γ were not linked with MMSE decline.ConclusionTh17 cells and IL‐17A estimate the progression of cognitive impairment in stroke patients.

Sleep habits are associated with cognition decline in physically robust, but not in frail participants: a longitudinal observational study

Frail older adults are vulnerable to stressors; thus, sleep related cognition impairment might more greatly affect frail than healthy older adults. In the present study, we investigated whether the association between sleep problems and cognition varies with physical frailty status (modified from Fried et al.). Participants 55 years and older who completed a baseline and follow-up questionnaire (median follow-up: 5.5 years), were included in the analysis. Sleep parameters were evaluated in an interview at the baseline. Cognitive decline was defined as a loss of 3 or more points on the Mini-Mental State Examination (MMSE) at follow-up. Associations between sleep problems and cognitive decline were examined using logistic regression and were stratified by baseline physical frailty status, adjusted for potential confounders. A short total sleep duration (< 5 vs. 7–9 h, odds ratio (OR) = 1.88, 95% confidence interval (CI) 1.18–3.00), excessive daytime sleepiness (OR = 1.49, 95% CI 1.04–2.13), low sleep efficiency (< 65% vs. ≥ 85%, OR = 1.62, 95% CI 1.07–2.46), and insomnia complaints (OR = 2.34, 95% CI 1.23–4.43) were associated with MMSE decline in physically robust. The association was stronger for the sleep summary score, which summarized abnormal sleep duration, excessive daytime sleepiness, and insomnia complaints (ge 2 vs. 0, OR = 3.79, 95% CI 2.10–6.85, p < 0.0001). Due to the low prevalence of frailty in this community-dwelling population, the statistical power to detect an association was low. More evidence is needed to clarify the role of sleep in the progression of cognitive decline in frail individuals.

Exploring the impact of community-based choral participation on cognitive function and well-being for persons with dementia: evidence from the Voices in Motion project

Objectives Music-based interventions are postulated to mitigate cognitive decline in individuals with dementia. However, the mechanisms underlying why music-based interventions facilitate cognitive benefits remain unknown. The present study examines whether a choral intervention can modulate patterns of cognitive change in persons with dementia and whether within-person variation in affect is associated with this change. Methods Thirty-three older adults with dementia engaged weekly in the Voices in Motion (ViM) study consisting of 3 choral seasons spanning 18-months. Performance on the Mini-Mental State Examination (MMSE) and the Positive and Negative Affect Schedule was assessed monthly within each choral season using a longitudinal intensive repeated-measures design. Three-level multilevel models were employed to disaggregate between- and within-person effects across short- (month-to-month) and long-term (season-to-season) intervals. Results ViM participants exhibited an annual MMSE decline of 1.8 units, notably less than the clinically meaningful 3.3 units indicated by non-intervention literature. Further, variability in negative affect shared a within-person time-varying association with MMSE performance; decreases in negative affect, relative to one’s personal average, were linked to corresponding improvements in cognitive function. Conclusion Engagement in the ViM choral intervention may attenuate cognitive decline for persons with dementia via a reduction of psychological comorbidities such as elevated negative affect.

Global cognitive trajectory patterns in Alzheimer's disease.

The literature on Alzheimer's disease (AD) provides little data about long-term cognitive course trajectories. We identify global cognitive outcome trajectories and associated predictor variables that may inform clinical research and care. Data derived from the National Alzheimer's Coordinating Center (NACC) Uniform Data Set were used to examine the cognitive course of persons with possible or probable AD, a Mini-Mental State Examination (MMSE) of ≥10, and complete annual assessments for 5 years. Thirty-six Alzheimer's Disease Research Centers. Four hundred and fourteen persons. We used a hybrid approach comprising qualitative analysis of MMSE trajectory graphs that were operationalized empiricallyand binary logistic regression analyses to assess 19 variables' associations with each trajectory. MMSE scores of ±3 points or greater were considered clinically meaningful. Five distinct cognitive trajectories were identified: fast decliners (32.6%), slow decliners (30.7%), zigzag stable (15.9%), stable (15.9%), and improvers (4.8%). The decliner groups had three subtypes: curvilinear, zigzag, and late decline. The fast decliners were associated with female gender, lower baseline MMSE scores, a shorter illness duration, or receiving a cognitive enhancer. An early MMSE decline of ≥3 points predicted a worse outcome. A higher rate of traumatic brain injury, the absence of an ApoE ϵ4 allele, and male gender were the strongest predictors of favorable outcomes. Our hybrid approach revealed five distinct cognitive trajectories and a variegated pattern within the decliners and stable/improvers that was more consistent with real-world clinical experience than prior statistically modeled studies. Future investigations need to determine the consistency of the distribution of these categories across settings.

Risk of cognitive impairment from exposure to incense smoke

ABSTRACT Incense is aromatic biotic material that releases fragrant smoke when burned. We aim to investigate the cognition risks from incense smoke. We obtained data from Taiwan Biobank in community. Cognition function was assessed by mini-mental state examination (MMSE). There were 978 participants in our study, including incense exposure (N = 131) and without incense exposure (N = 847). MMSE scores and registration sub-scores were lowered in incense exposure group than the other group. Incense exposure is one of the independent risk factors for cognitive decline in MMSE and registration sub-scores after adjusting confounding factors We concluded the risk of cognitive impairment, with predominant in registration in healthy individuals with incense exposure in community.

White matter hyperintensities in the splenium of the corpus callosum predict cognitive decline in memory clinic outpatients

AbstractBackgroundWhite matter hyperintensities (WMH) are very frequent in ageing and related to worse cognition. Recent studies suggest that WMH in the corpus callosum (CC) are particularly relevant in neurocognitive disorders, as they are strongly associated with lower cognitive performance, as well as amyloid and neurodegeneration biomarkers. This study examined whether WMH in subregions of the CC (genu, body, splenium) affect cross‐sectional and long‐term longitudinal (up to 5 years) cognitive performance in patients recruited from a memory clinic.MethodThis study included memory clinic outpatients from the MEMORA cohort who had a brain MRI (T1 and FLAIR scans) within 6 months of the baseline visit. QyScore® software was used for the automatic segmentation of WMH in the CC and hippocampal volumes (HP). The cross‐sectional and longitudinal relationships between regional WMH in the CC and cognitive performance, as measured with the mini‐mental state examination (MMSE), were assessed using multivariable linear regressions and mixed models.ResultAmong 236 patients included (mean age 76.2±8.8 years old; mean MMSE 23.6±4.9), 111 were diagnosed with probable Alzheimer’s disease (AD), 20 with vascular cognitive impairment (VCI), 22 with mixed AD‐VCI, 18 with another neurological disease and 65 with a subjective cognitive complaint. Cross‐sectional analyses disclosed that higher WMH in the splenium of the CC were associated with reduced MMSE (p=0.03, n=199) after adjustment for diagnosis and education. The relationship did not remain significant after adjustment for HP and total WMH. Longitudinal analyses with a follow‐up up to 5 years showed that the MMSE declined faster in patients with higher WMH in the splenium of the CC (p&lt;0.001, n=143) after adjustment for education, diagnosis, HP and total WMH (Figure). WMH in the genu and in the body of the CC were not associated with MMSE decline (respectively p=0.92 and p=0.23, n=124, Figure).ConclusionWMH in the splenium of the CC were associated with cognitive decline, whereas WMH in the genu and the body were not. This study highlights the clinical relevance of posterior CC WMH in a memory clinic population.

Evaluation of blood pressure and cognitive function using individual participant data meta‐analysis: The Life‐Course Blood Pressure Cognition (LCBP‐COG) study

AbstractBackgroundThe prognostic significance of various blood pressure (BP) indices (i.e. systolic BP [SBP], diastolic BP [DBP], pulse pressure [PP] and mean arterial pressure [MAP]) on cardio‐ and cerebrovascular health vary across age groups. We examined the association between baseline BP indices in mid‐ and late‐life and cognitive function over a 9‐15 year period.MethodWe performed pooled analyses of data from 3 longitudinal cohort studies. The Personality and Total Health (PATH) Through Life study of adults initially aged 40‐44 and 60‐64 years in Australia, and Victoria Longitudinal Study (VLS) of adults initially aged 55‐85 years in Canada, included four waves of data collection every 4‐5 years. The Gothenburg H70 Birth cohort study of adults initially aged 70 years included three waves of data collection every 4‐5 years. The association between baseline BP and cognitive decline on the Mini‐Mental State Examination (MMSE) was categorized using the reliable change index (Duff K. 2012) and analyzed using logistic regression adjusted for age, sex, and study. Additional analyses examined relationships between baseline BP and repeated cognitive measures of memory, attention and processing speed, and executive function, using linear mixed models (PATH and H70). Only participants with complete BP and cognitive measures were included.ResultData from 2912 participants (mean baseline age 54.3 years, range 40 to 83 years, 1395 (47.9%) male) were included. Examining baseline BP and age, we observed SBP increasing with age until a small decrease at around 80 years. DBP and MAP also showed an increase with age until early late‐life (around 60 years) and were lower at older ages, PP consistently increased (Figure 1). There were no relationships between baseline BP measures and MMSE. For PATH only, higher SBP (P=0.002), DBP (P=0.0007) and MAP (P=0.0006) at age 40 years, and higher DBP (P=0.004) at 60 years, were associated with greater annual deterioration in attention and processing speed (symbol‐digit‐modalities test) over the subsequent decade (Figure 2).ConclusionHigher BP in midlife and DBP in early late‐life, were associated with a greater decline in measures of attention and processing speed. We observed no associations between BP and MMSE decline.