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Background: There is a need to better understand the rate of cognitive and motor decline of Dementia with Lewy bodies (DLB) and Parkinson's disease Dementia (PDD). Objectives: To compare the rate of cognitive and motor decline in patients with DLB and PDD from the E‐DLB Consortium and the Parkinson's Incidence Cohorts Collaboration (PICC) Cohorts. Methods: The annual change in MMSE and MDS‐UPDRS part III was estimated using linear mixed regression models in patients with at least one follow‐up (DLB n = 837 and PDD n = 157). Results: When adjusting for confounders, we found no difference in the annual change in MMSE between DLB and PDD (−1.8 [95% CI −2.3, −1.3] vs. −1.9 [95% CI −2.6, −1.2] [P = 0.74]). MDS‐UPDRS part III showed nearly identical annual changes (DLB 4.8 [95% CI 2.1, 7.5]) (PDD 4.8 [95% CI 2.7, 6.9], [P = 0.98]). Conclusions: DLB and PDD showed similar rates of cognitive and motor decline. This is relevant for future clinical trial designs. [ABSTRACT FROM AUTHOR]

Background and Aims: In older adults with dementia, low body mass index (BMI) is associated with higher mortality and other adverse health outcomes. BMI or nutritional status trajectories from diagnosis have not yet been well described in dementia, especially in people with Lewy body dementia (LBD); a group that has a poorer prognosis. With this study, we aimed to evaluate the BMI trajectory in people diagnosed with mild LBD and Alzheimer's disease (AD). Methods: The Dementia Study of Western Norway is a cohort study with annual assessments. Five‐year measurements of BMI from 196 patients (LBD = 85 and AD = 111) diagnosed with mild dementia were analyzed using adjusted linear mixed‐effects models. Results: There were no differences between LBD and AD in baseline BMI, age, or mini‐mental status examination (MMSE). During the follow‐up, we observed a significant decrease in BMI in the LBD group across the study period (estimation [Est.]: −0.63, SE: 0.14; p < 0.001). By contrast, there was no significant change in BMI trajectory associated with AD diagnosis (Est.: 0.05, SE: 0.15; p = 0.730). Further, the introduction of an interaction term between diagnosis and time in the study showed that this difference (BMI trajectories) was significant (Est.: −0.63, SE: 0.14; p < 0.001). In addition, there was a significant interaction between MMSE total score and the follow‐up time; the lower the MMSE, the lower the BMI (Est.: 0.01, SE: 0.01; p = 0.044). Conclusion: In LBD, BMI significantly decreased with disease progression. In addition, low cognitive performance was associated with a reduction in BMI. These results highlight the importance of BMI evaluation in people with dementia, particularly patients diagnosed with LBD, and suggest that patients with LBD could be targeted for dietary intervention to maintain body weight. [ABSTRACT FROM AUTHOR]

Malnutrition is highly prevalent in older persons with dementia. Therefore, strong predictors of malnutrition in this population are crucial to initiating early interventions. This study evaluates the association between the probability of having malnutrition with the muscle volume and intramuscular fat (iMAT) of the masseter and the tongue in magnetic resonance imaging (MRI) of community-dwelling older persons diagnosed with mild dementia followed up for 5 years. This is a longitudinal study conducted in the western part of Norway. Muscle volume and iMAT of the tongue and masseter were computed from structural head MRI obtained from 65 participants of the Dementia Study of Western Norway using Slice-O-Matic software for segmentation. Malnutrition was assessed using the Global Leadership Initiative on Malnutrition Index. Linear mixed models were conducted. Having malnutrition at baseline was associated with lower muscle volume (odds ratio [OR] 0.60, standard error [SE] 0.20; p = .010) and higher iMAT (OR 3.31, SE 0.46; p = .010) in the tongue. At 5 years follow-up, those with lower muscle volume (OR 0.55, SE 0.20; p = .002) and higher iMAT (OR 2.52, SE 0.40; p = .022) in the tongue had a higher probability of presenting malnutrition. The masseter iMAT and volume were not associated with malnutrition in any of the adjusted models. In people diagnosed with mild dementia, tongue muscle volume and iMAT were associated with baseline malnutrition and the probability of developing malnutrition in a 5-year trajectory. In the masseter, there were no significant associations after adjustments. [ABSTRACT FROM AUTHOR]

Introduction: The amygdala is implicated in psychiatric illness. Even as the amygdala undergoes significant atrophy in mild dementia, amygdala volume is underexplored as a risk factor for neuropsychiatric symptoms (NPS). Objective: To analyze the association between baseline amygdala volume and the longitudinal trajectories of NPS and cognitive decline in Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) over 5 years. Methods: Eighty-nine patients with mild dementia were included (AD = 55; DLB = 34). Amygdala volume was segmented from structural magnetic resonance images (sMRI) using a semi-automatic method (Freesurfer 6.0) and normalized by intracranial volumes. The intracranial volume-normalized amygdala was used as a predictor of the Neuropsychiatric Inventory (NPI) total score, ordinal NPI item scores (0 = absence of symptoms, 1–3 = mild symptoms, ≥4 = clinically relevant symptoms), and Mini-Mental State Examination (MMSE) as measured annually over 5 years using gamma, ordinal, and linear mixed-effects models, respectively. The models were adjusted for demographic variables, diagnosis, center of sMRI acquisition, and cognitive performance. Multiple testing-corrected p -values (q -values) are reported. Results: Larger intracranial volume-normalized amygdala was associated with less agitation/aggression (odds ratio (OR) = 0.62 [0.43, 0.90], p = 0.011, q = 0.038) and less MMSE decline per year (fixed effect = 0.70, [0.29, 1.03], p = 0.001, q = 0.010) but more depression (OR = 1.49 [1.09, 2.04], p = 0.013, q = 0.040). Conclusions: Greater amygdala volume in mild dementia is associated with lower odds of developing agitation/aggression, but higher odds of developing depression symptoms during the 5-year study period. [ABSTRACT FROM AUTHOR]

Objectives: We aim to study the effects of the prescription of benzodiazepines and antidepressants on cognitive and functional decline in older adults living with Alzheimer's disease (AD) and Lewy body dementia (LBD) over a 5‐year follow‐up. Methods: This is a longitudinal analysis of a Norwegian cohort study entitled "The Dementia Study of Western Norway" (DemVest). We included 196 patients newly diagnosed with AD (n = 111) and LBD (n = 85), followed annually for 5 years. Three prescription groups were defined: only benzodiazepines (BZD), only antidepressants (ADep), and the combination of benzodiazepines and antidepressants (BZD‐ADep). Linear mixed‐effects models were conducted to analyze the effect of the defined groups on the outcomes. The outcomes were functional decline, measured by the Rapid Disability Rating Scale—2, and cognition measured with the Mini‐Mental State Examination. Results: Prescription of the combination of benzodiazepines and antidepressants in LBD was associated with faster functional decline. In AD, the prescription of BZD and BZD‐ADep was associated with greater functional deterioration. ADep alone did not show positive or negative significant associations with the studied outcomes. Conclusions: BZD and especially the combination of BZD and ADep are associated with functional decline in AD and LBD and should be used cautiously. Key Points: Combination of benzodiazepines and antidepressants in Lewy body dementia was associated with faster functional declineBenzodiazepines and the combination of benzodiazepines and antidepressants in Alzheimer's disease were associated with greater functional deteriorationThe consumption of antidepressants alone did not show positive or negative significant associations with cognitive or functional decline [ABSTRACT FROM AUTHOR]

Background: In dementia, functional status depends on multiple factors in addition to cognition. Nutritional status is a potentially modifiable factor related to homeostasis and proper functioning of body systems and may contribute to cognitive and functional decline.Objective: This paper aims to analyze the association of malnutrition with the course of cognitive and functional decline in people living with dementia.Methods: This is an analysis of a longitudinal cohort study, the Dementia Study of Western Norway. Data of 202 patients diagnosed with mild dementia were analyzed; Alzheimer's disease (AD) (n = 103), Lewy body dementia (LBD) (n = 74), and other dementias (OD) (n = 25). Cognition was assessed with the Mini-Mental State Examination and functional decline through the activities of daily living included in the Rapid Disability Rating Scale. The Global Leadership Initiative on Malnutrition Index was used to determine nutritional status. Associations of nutritional status with cognitive and functional decline were evaluated through adjusted linear mixed models.Results: At baseline, the prevalence of general malnutrition was 28.7%; 17.3% were classified as moderate malnutrition and 11.38% as severe malnutrition (there were no significant differences between AD and LBD). Malnutrition at diagnosis and over follow-up was a significant predictor of functional-decline, but not of cognitive decline.Conclusion: According to our results malnutrition was associated with faster functional loss but, not cognitive decline in older adults with dementia. A more comprehensive dementia approach including nutritional assessments could improve prognosis. [ABSTRACT FROM AUTHOR]

BACKGROUND/OBJECTIVES Functional status is one of the most important markers of well‐being in older adults, but the drivers of functional decline in dementia are not well known. The aim of our work was to study the association of neuropsychiatric symptoms (NPSs) with functional decline over 5 years in newly diagnosed people with Alzheimer´s disease (AD) and Lewy body dementia (LBD). DESIGN Secondary analysis of the Dementia Study of Western Norway longitudinal cohort study. SETTING Multicenter study conducted in memory clinics in western Norway. PARTICIPANTS We included a total of 196 patients newly diagnosed with AD (n = 111) and LBD (n = 85), followed up annually for 5 years. MAIN OUTCOMES AND MEASURES The outcome was the rapid disability rating scale (items 1–13). Linear mixed‐effects models were used for analysis with the total score of the Norwegian Neuropsychiatric Inventory (NPI) as a predictor measured either at baseline or longitudinally, adjusted for potential confounders, including cognition. Effect modification was checked by introducing interactions with NPI score and stratifying by diagnosis. RESULTS: The total NPI score longitudinal course was associated with functional decline in both AD and LBD. At baseline, the total NPI score predicted functional decline in AD. CONCLUSION: NPSs were associated with the rate of functional decline in people with AD and LBD, independent of cognitive impairment. These results highlight the relevance of early detection and intervention of NPSs, which may also reduce functional decline. J Am Geriatr Soc 68:2257–2263, 2020. [ABSTRACT FROM AUTHOR]

• Serum citrate concentrations in mild dementia could be associated with subsequent cognitive decline. • In mild dementia APOE- ε4 carriers, serum isocitrate concentrations could be associated with subsequent cognitive decline. • Downregulation of the first half of the TCA cycle with upregulation in the latter half, might be indirectly reflected in serum metabolites' networks. Abnormalities in the Tri-Carboxylic-Acid (TCA) cycle have been documented in dementia. Through network analysis, TCA cycle metabolites could indirectly reflect known dementia-related abnormalities in biochemical pathways, and key metabolites might be associated with prognosis. This study analyzed TCA cycle metabolites as predictors of cognitive decline in a mild dementia cohort and explored potential interactions with the diagnosis of Lewy Body Dementia (LBD) or Alzheimer's Disease (AD) and APOE-ε4 genotype. We included 145 mild dementia patients (LBD = 59; AD = 86). Serum TCA cycle metabolites were analyzed at baseline, and partial correlation networks were conducted. Cognitive performance was measured annually over 5-years with the Mini-mental State Examination. Longitudinal mixed-effects Tobit models evaluated each baseline metabolite as a predictor of 5-years cognitive decline. APOE-ε4 and diagnosis interactions were explored. Results showed comparable metabolite concentrations in LBD and AD. Multiple testing corrected networks showed larger coefficients for a negative correlation between pyruvate – succinate and positive correlations between fumarate – malate and citrate – Isocitrate in both LBD and AD. In the total sample, adjusted mixed models showed significant associations between baseline citrate concentration and longitudinal MMSE scores. In APOE-ε4 carriers, baseline isocitrate predicted MMSE scores. We conclude that, in mild dementia, serum citrate concentrations could be associated with subsequent cognitive decline, as well as isocitrate concentrations in APOE-ε4 carriers. Downregulation of enzymatic activity in the first half of the TCA cycle (decarboxylating dehydrogenases), with upregulation in the latter half (dehydrogenases only), might be indirectly reflected in serum TCA cycle metabolites' networks. [ABSTRACT FROM AUTHOR]

• Sarcopenia and dementia are two of the most important conditions in old age. • Traditional brain MRI offers a novel approach to muscular assessment in patients with dementia. • Tongue muscle quantification is a novel and practical approach for muscle mass assessment in dementia. • Tongue muscle mass is associated with grey matter and hippocampal volumes in Dementia with Lewy Bodies. • In dementia, muscle condition could be more systematically measured using tongue muscle. Age-related neurodegeneration, sarcopenia, and ectopic fat accumulation are conditions with shared pathways that remain poorly understood. We have measured muscle volume and fat accumulation in masseter and tongue muscle, and aim to explore their association with the total grey matter volume using MRI in older adults recently diagnosed with Alzheimer's disease (AD) and Dementia with Lewy bodies (DLB). In this cross-sectional study, people newly diagnosed with mild AD (n=33) and DLB (n=20) underwent structural head MRI. Muscle volume and intramuscular fat (iMAT) of the tongue and masseter were computed using Slice-O-Matic software for segmentation. Total grey volume and hippocampal volumetric segmentation were performed with the FreeSurfer image analysis suite version 6.0. Independent regression models were employed to analyse the associations. Tongue iMAT was higher and total grey volume lower in DLB compared to AD. In the DLB group, tongue muscle was positively associated with total grey matter volume Est 0.92 (SE 0.24 p -value 0.002), left- Est 0.01 (SE 0.0028 p -value 0,002), and right- Est 0.0088 (SE 0.0027 p -value: 0.005) hippocampal volume. There were no statistically significant results for AD. Tongue muscle volume was positively associated with hippocampal and total grey volume in DLB. Longitudinal designs are required to explore the extent and significance of this association. [ABSTRACT FROM AUTHOR]

• Patients with Lewy body dementia were prescribed a higher number of medications than those with Alzheimer's disease. The mean number increased in both groups during follow up. • We found in both types of dementia a faster functional decline related to the number of prescribed medications • The Number of prescribed medications was not associated with cognitive decline In dementia, a number of factors may influence functional decline in addition to cognition. In this study, we aimed to study the potential association of the number of prescribed medications with functional decline trajectories over a five-year follow-up in people diagnosed with mild Alzheimer's disease (AD) or Lewy Body dementia (LBD). This is a longitudinal analysis of a Norwegian cohort study entitled "The Dementia Study of Western Norway". We included 196 patients newly diagnosed with AD (n=111) and LBD (n=85), followed annually for 5 years. We conducted linear mixed-effects models to analyse the association of the number of medications with functional decline measured by the Rapid Disability Rating Scale – 2. The mean prescribed medications at baseline was 4.18∓2.60, for AD 3.92∓2.51 and LBD 4.52∓2.70. The number of medications increased during the follow-up; at year five the mean for AD was 7.28∓4.42 and for LBD 8.11∓5.16. Using more medications was associated with faster functional decline in AD (Est 0.04, SE 0.01, p-value 0.003) and LBD (Est 0.08, SE 0.03, p-value 0.008) after adjusting for age, sex, comorbidity, neuropsychiatric symptoms, and cognition. For each medication added during the follow-up, functional trajectories worsened by 1% for AD and 2% for LBD. The number of medications was not associated with cognitive decline. We found that higher number of medications was related to a faster functional decline, both in AD and LBD. With disease progression, there was an increase in the number of medications. Prescription in dementia should be carefully assessed, possibly improving the functional prognosis. [ABSTRACT FROM AUTHOR]