BACKGROUND: Although neuromelanin-sensitive magnetic resonance imaging (NM-MRI) has been used to evaluate early neurodegeneration in Parkinson's disease, studies concentrating on the locus coeruleus (LC) in pre-dementia stages of dementia with Lewy bodies (DLB) are lacking. OBJECTIVES: The aims were to evaluate NM-MRI signal changes in the LC in patients with mild cognitive impairment with Lewy bodies (MCI-LB) compared to healthy controls (HC) and to identify the cognitive correlates of the changes. We also aimed to test the hypothesis of a caudal-rostral α-synuclein pathology spread using NM-MRI of the different LC subparts. METHODS: A total of 38 MCI-LB patients and 59 HCs underwent clinical and cognitive testing and NM-MRI of the LC. We calculated the contrast ratio of NM-MRI signal (LC-CR) in the whole LC as well as in its caudal, middle, and rostral MRI slices, and we compared the LC-CR values between the MCI-LB and HC groups. Linear regression analyses were performed to assess the relationship between the LC-CR and cognitive outcomes. RESULTS: The MCI-LB group exhibited a significant reduction in the right LC-CR compared to HCs (P = 0.021). The right LC-CR decrease was associated with impaired visuospatial memory in the MCI-LB group. Only the caudal part of the LC exhibited significant LC-CR decreases in MCI-LB patients compared to HCs on both sides (P < 0.0001). CONCLUSIONS: This is the first study that focuses on LC-CRs in MCI-LB patients and analyzes the LC subparts, offering new insights into the LC integrity alterations in the initial stages of DLB and their clinical correlates. © 2024 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

• MeSH
• alpha-Synuclein metabolism   MeSH
• Lewy Body Disease * diagnostic imaging   pathology   MeSH
• Cognitive Dysfunction * diagnostic imaging   pathology   physiopathology   etiology   MeSH
• Middle Aged MeSH
• Humans MeSH
• Locus Coeruleus * diagnostic imaging   pathology   MeSH
• Magnetic Resonance Imaging * MeSH
• Neuropsychological Tests MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

Cíl: Montrealský kognitivní test (MoCA) je jednou z nejpoužívanějších screeningových zkoušek kognice u dospělých osob, pro něž existují normy pro českou populaci. Varianta MoCA-22, která je určena pro osoby s poruchami zraku či imobilitou horních končetin, se dá administrovat i po telefonu. Tato studie přináší české normy MoCA-22. Materiál a metodika: Soubor (n = 1 049) se skládá z účastníků čtyř studií provedených v ČR. Zařazeny byly osoby ve věku 19–98 let, bez neurodegenerativního, psychiatrického či jiného závažného onemocnění. Data pro MoCA-22 byla odvozena z dat získaných vyšetřením standardní verzí MoCA. V souladu se zavedenou klinickou praxí i statistickou analýzou jsou soubor a odvozené normy rozděleny na tři věkové kategorie: 19–50 let, 51–74 let, 75 a více let. Výsledky: Pro výše uvedené věkové kategorie dále rozdělené dle dosaženého vzdělání (nižší, vyšší) předkládáme průměrné skóry i odhadované percentilové hranice. Výkon v MoCA-22 je ovlivněn dosaženým vzděláním a věkem, ale nikoli pohlavím. Pro úpravu výsledků dle demografických faktorů proto poskytujeme i regresní rovnici. Závěr: Normativní údaje pro MoCA-22 rozšíří klinické instrumentárium v Česku a umožní adekvátní screening kognice u osob, jež jsou zdravotním stavem limitovány při využití standardních metod.

Aim: The Montreal Cognitive Assessment (MoCA) is one of the most widely used cognitive screening tests in adults with reference standards for the Czech population. The MoCA-22 variant is designed for individuals with visual impairment or upper limb immobility and can be administered over the telephone. This study presents the Czech MoCA-22 normative standards. Materials and methods: The sample (N = 1,049) consists of participants from four studies conducted in the Czech Republic. The subjects included were aged 19–98 years, and were without neurodegenerative, psychiatric, or other serious illness. Data for the MoCA-22 were derived from data obtained by the standard version of MoCA. Following established clinical practice and statistical analysis, the population and derived norms are divided into three age categories: 19–50 years, 51–74 years, and 75 years and older. Results: For these age categories above, which were further subdivided by educational status (lower, higher), we present mean scores and estimated percentile thresholds. Performance in the MoCA-22 is affected by demoraphic factors, such as educational status and age but not sex, as reflected by the regression equation. Conclusions: Normative data for MoCA-22 will complement the clinical armamentarium in Czechia and allow adequate cognitive screening in people whose health status limits them when using standard methods.

• Keywords
• Montrealský kognitivní test (MoCA),
• MeSH
• Clinical Studies as Topic MeSH
• Cognition Disorders diagnosis   MeSH
• Humans MeSH
• Neuropsychological Tests * standards   MeSH
• Bedridden Persons MeSH
• Telephone MeSH
• Telemedicine MeSH
• Persons with Visual Disabilities MeSH
• Check Tag
• Humans MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH

BACKGROUND: Cognitive impairment is a well-recognized symptom of multiple sclerosis (MS) that can manifest early in the disease course. Deficits in cognitive function can have a major impact on daily life. However, cognitive decline is often under-examined in clinical trials and clinical practice due to lack of adequate data. The objective of this study was to examine the longitudinal effect of ocrelizumab vs interferon beta (IFNβ)-1a on cognitive impairment in 2 phase 3 studies in relapsing MS (RMS). METHODS: The pooled population of participants with RMS (n = 1656) from the OPERA I/II clinical trials received subcutaneous IFNβ-1a (44 μg; n = 829) 3 times weekly or intravenous ocrelizumab (600 mg; n = 827) every 24 weeks. Cognition was assessed with a Symbol Digit Modalities Test (SDMT), administered in written or oral form according to each site investigator's choice, that primarily measured cognitive processing speed at baseline and every 12 weeks until the end of the double-blind treatment (96 weeks). Treatment effects were investigated based on longitudinal linear models for the change from baseline in SDMT and Cox regression for the time to 12- or 24-week confirmed decline of ≥4 points. RESULTS: Among the participants with an SDMT assessment at baseline and ≥1 postbaseline time point (IFNβ-1a, n = 749; ocrelizumab, n = 766), ocrelizumab treatment was associated with a greater mean SDMT improvement over 96 weeks than IFNβ-1a treatment (5.4 [95 % CI, 4.4-6.5] vs 4.0 [95 % CI, 3.0-5.1]; adjusted mean difference, 1.4 [95 % CI, 0.05-2.72]; P = 0.042). The risk of a clinically meaningful SDMT decline (≥4 points) was lower for those treated with ocrelizumab for both ≥12 weeks (IFNβ-1a, 18.4 %; ocrelizumab, 12.7 %; hazard ratio, 0.63 [95 % CI, 0.47-0.85]; P = 0.003) and ≥24 weeks (IFNβ-1a, 12.9 %; ocrelizumab, 7.9 %; HR, 0.57 [95 % CI, 0.39-0.82]; P = 0.003). CONCLUSION: Ocrelizumab treatment resulted in better cognitive outcomes as measured by SDMT in participants with RMS compared with IFNβ-1a treatment. However, methodological limitations need to be considered when interpreting these data. CLINICALTRIALS: gov: NCT01247324, NCT01412333.

• MeSH
• Adult MeSH
• Double-Blind Method MeSH
• Antibodies, Monoclonal, Humanized * administration & dosage   pharmacology   adverse effects   MeSH
• Immunologic Factors * administration & dosage   adverse effects   pharmacology   MeSH
• Interferon beta-1a * administration & dosage   pharmacology   MeSH
• Cognitive Dysfunction etiology   drug therapy   chemically induced   MeSH
• Middle Aged MeSH
• Humans MeSH
• Longitudinal Studies MeSH
• Multiple Sclerosis, Relapsing-Remitting * drug therapy   MeSH
• Treatment Outcome MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Clinical Trial, Phase II MeSH
• Clinical Trial, Phase III MeSH
• Randomized Controlled Trial MeSH
• Comparative Study MeSH

Pochopení vztahu mezi senzomotorickými proměnnými a exerkiny, které ovlivňují funkci mozku a kognici, nám umožňuje hlouběji porozumět biologickému procesu stárnutí. Hlavním cílem této studie bylo zjistit, jak silně jsou mozkový neurotrofický faktor (brain-derived neurotrophic factor, BDNF), irisin, svalová hmota a svalová síla asociovány s výsledky testů vybraných kognitivních funkcí u starších žen a jak dobře je predikují. Padesát sedm starších žen (průměrný věk 70,4 ± 4,1 roku) absolvovalo baterii neuropsychologických testů, měření izometrické dynamometrie a bioelektrické impedance. Hladiny v krevním séru sledovaných exerkinů byly stanoveny enzymatickým imunosorbentním testem (ELISA). Pro testování predikcí byly využity hierarchické vícenásobné regresní modely. Odhadli jsme, že rozptyl 46,1 % v krátkodobé paměti byl zapříčiněn hladinami BDNF v séru, přičemž druhým statisticky významným prediktorem byl věk (beta = –0,22; p = 0,030). Síla dolních končetin (lower limb strength, LLS) prokázala významnou prediktivní sílu jak u paměti – bezprostřední vybavení (beta = 0,39; p = 0,004), tak u paměti – oddálené vybavení (beta = 0,45; p = 0,001). Hladiny BDNF v séru byly významným prediktorem u oddáleného vybavení (beta = 0,29; p = 0,048). Přidání hladin BDNF do modelu prokázalo významné zvýšení jeho prediktivní síly o přibližně 5,6 % (p = 0,048) u paměti – oddálené vybavení. Index kosterní svalové hmoty (skeletal muscle index, SMI) a úroveň vzdělání byly významnými prediktory mentální flexibility. Byla zjištěna silná pozitivní asociace mezi hladinami BDNF, irisinem, svalovou silou a kognitivní funkcí, přičemž irisin a svalová síla jsou silnými prediktory hladin BDNF u starších žen. Studie byla realizována s podporou grantu Univerzity Karlovy – PRIMUS/19/HUM/012, Specifického vysokoškolského výzkumu SVV 260599, projektu COOPERATIO a Grantové agentury UK číslo grantu 268321. Korespondenční adresa: PhDr. Veronika Holá Katedra gymnastiky a úpolových sportů FTVS UK José Martího 269/31 162 52 Praha 6-Veleslavín e-mail: veronika.hola@ftvs.cuni.cz

Understanding the relationship between sensorimotor variables and exerkines related to brain function and cognition may help better understand biological ageing. The main aim of this study was to determine how strongly brain-derived neurotrophic factor (BDNF), irisin, muscle mass and muscle strength are associated and predict scores on selected cognitive domain tests in older women. Fifty seven older women (mean age 70.4 ± 4.1 years) underwent a battery of cognitive and psychological tests and measurements of isometric dynamometry and bioelectrical impedance. Serum exerkines levels were measured by enzyme-linked immunosorbent assay (ELISA). Hierarchical multiple regression models were used to test the predictions. We estimated that 46.1% of the variance in short-term memory was accounted for by serum BDNF levels, with age being the second statistically significant predictor (Beta = -0.22; p = 0.030). Lower limb strength (LLS) showed significant predictive power in both immediate (Beta = 0.39; p = 0.004) and delayed memory (Beta = 0.45; p = 0.001), serum BDNF levels were a significant predictor in delayed memory (Beta = 0.29; p = 0.048). Adding serum BDNF levels to the model showed a significant increase in predictive power of approximately 5.6% (p = 0.048) in delayed memory. Skeletal muscle index (SMI) and education level were significant predictors of mental flexibility. A strong positive association between BDNF levels, irisin, muscle strength, and cognitive function was found, with irisin and muscle strength being strong predictors of BDNF levels in older women.

• Keywords
• irisin,
• MeSH
• Fibronectin Type III Domain physiology   MeSH
• Cognition physiology   MeSH
• Cognitive Aging * physiology   MeSH
• Humans MeSH
• Brain-Derived Neurotrophic Factor blood   MeSH
• Neuropsychological Tests * statistics & numerical data   MeSH
• Memory physiology   MeSH
• Prognosis MeSH
• Cross-Sectional Studies MeSH
• Regression Analysis MeSH
• Aged MeSH
• Muscular Atrophy etiology   MeSH
• Muscle Strength physiology   MeSH
• Check Tag
• Humans MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH

OBJECTIVE: This study aims to evaluate the efficacy of the Uniform Data Set (UDS) 2 battery in distinguishing between individuals with mild cognitive impairment (MCI) attributable to Alzheimer's disease (MCI-AD) and those with MCI due to other causes (MCI-nonAD), based on contemporary AT(N) biomarker criteria. Despite the implementation of the novel UDS 3 battery, the UDS 2 battery is still used in several non-English-speaking countries. METHODS: We employed a cross-sectional design. A total of 113 Czech participants with MCI underwent a comprehensive diagnostic assessment, including cerebrospinal fluid biomarker evaluation, resulting in two groups: 45 individuals with prodromal AD (A+T+) and 68 participants with non-Alzheimer's pathological changes or normal AD biomarkers (A-). Multivariable logistic regression analyses were employed with neuropsychological test scores and demographic variables as predictors and AD status as an outcome. Model 1 included UDS 2 scores that differed between AD and non-AD groups (Logical Memory delayed recall), Model 2 employed also Letter Fluency and Rey's Auditory Verbal Learning Test (RAVLT). The two models were compared using area under the receiver operating characteristic curves. We also created separate logistic regression models for each of the UDS 2 scores. RESULTS: Worse performance in delayed recall of Logical Memory significantly predicted the presence of positive AD biomarkers. In addition, the inclusion of Letter Fluency RAVLT into the model significantly enhanced its discriminative capacity. CONCLUSION: Our findings demonstrate that using Letter Fluency and RAVLT alongside the UDS 2 battery can enhance its potential for differential diagnostics.

• MeSH
• Alzheimer Disease * diagnosis   cerebrospinal fluid   MeSH
• Amyloid beta-Peptides cerebrospinal fluid   MeSH
• Biomarkers * cerebrospinal fluid   MeSH
• Diagnosis, Differential MeSH
• Cognitive Dysfunction * diagnosis   etiology   MeSH
• Middle Aged MeSH
• Humans MeSH
• Neuropsychological Tests * standards   statistics & numerical data   MeSH
• tau Proteins cerebrospinal fluid   MeSH
• Cross-Sectional Studies MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

BACKGROUND: Genetic variations in a common single nucleotide polymorphism in the ninth intron of the KIBRA gene have been linked to memory performance and risk of Alzheimer's disease (AD). OBJECTIVE: We examined the risk of AD related to presence of KIBRA T allele (versus CC homozygote) and to memory performance. The role of established genetic risk factors APOE ε4 and BDNF Met was also considered. METHODS: Participants were cognitively healthy individuals (n = 19), participants with amnestic mild cognitive impairment (aMCI) due to AD (n = 99) and AD dementia (n = 37) from the Czech Brain Aging Study. Binary and multinomial logistic regressions compared odds of belonging to a certain diagnostic category and multivariate linear regressions assessed associations with memory. RESULTS: KIBRA T allele was associated with increased AD dementia risk (odds ratio [OR] = 5.98, p = 0.012) compared to KIBRA CC genotype. In APOE ε4 negative individuals, KIBRA T allele was associated with a greater risk of both aMCI due to AD (OR = 6.68, p = 0.038) and AD dementia (OR = 15.75, p = 0.009). In BDNF Met positive individuals, the KIBRA T allele was associated with a greater risk of AD dementia (OR = 10.98, p = 0.050). In AD dementia, the association between KIBRA T allele and better memory performance approached significance (β = 0.42; p = 0.062). The link between possessing the KIBRA T allele and better memory reached statistical significance only among BDNF Met carriers (β = 1.21, p = 0.027). CONCLUSIONS: Findings suggest that KIBRA T allele may not fully protect against AD dementia but could potentially delay progression of post-diagnosis cognitive deficits.

• MeSH
• Alleles MeSH
• Alzheimer Disease * genetics   MeSH
• Apolipoprotein E4 genetics   MeSH
• Genetic Predisposition to Disease genetics   MeSH
• Genotype MeSH
• Intracellular Signaling Peptides and Proteins genetics   MeSH
• Polymorphism, Single Nucleotide * genetics   MeSH
• Cognitive Dysfunction * genetics   MeSH
• Humans MeSH
• Brain-Derived Neurotrophic Factor genetics   MeSH
• Neuropsychological Tests MeSH
• Memory physiology   MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

BACKGROUND: There is initial evidence suggesting that biomarker neurogranin (Ng) may distinguish Alzheimer's disease (AD) from other neurodegenerative diseases. Therefore, we assessed (a) the discriminant ability of cerebrospinal fluid (CSF) Ng levels to distinguish between AD and frontotemporal lobar degeneration (FTLD) pathology and between different stages within the same disease, (b) the relationship between Ng levels and cognitive performance in both AD and FTLD pathology, and (c) whether CSF Ng levels vary by apolipoprotein E (APOE) polymorphism in the AD continuum. METHODS: Participants with subjective cognitive decline (SCD) (n = 33), amnestic mild cognitive impairment (aMCI) due to AD (n = 109), AD dementia (n = 67), MCI due to FTLD (n = 25), and FTLD dementia (n = 29) were recruited from the Czech Brain Aging Study. One-way analysis of covariance (ANCOVA) assessed Ng levels in diagnostic subgroups. Linear regressions evaluated the relationship between CSF Ng levels, memory scores, and APOE polymorphism. RESULTS: Ng levels were higher in aMCI-AD patients compared to MCI-FTLD (F[1, 134] = 15.16, p < .001), and in AD-dementia compared to FTLD-dementia (F[1, 96] = 4.60, p = .029). Additionally, Ng levels were higher in FTLD-dementia patients compared to MCI-FTLD (F[1, 54]= 4.35, p = .034), lower in SCD participants compared to aMCI-AD (F[1, 142] = 10.72, p = .001) and AD-dementia (F[1, 100] = 20.90, p < .001), and did not differ between SCD participants and MCI-FTLD (F[1, 58]= 1.02, p = .491) or FTLD-dementia (F[1, 62]= 2.27, p = .051). The main effect of diagnosis across the diagnostic subgroups on Aβ1-42/Ng ratio was significant too (F[4, 263]=, p < .001). We found a non-significant association between Ng levels and memory scores overall (β=-0.25, p = .154) or in AD diagnostic subgroups, and non-significant differences in this association between overall AD APOE ε4 carriers and non-carriers (β=-0.32, p = .358). CONCLUSIONS: In this first study to-date to assess MCI and dementia due to AD or FTLD within one study, elevated CSF Ng appears to be an early biomarker of AD-related impairment, but its role as a biomarker appears to diminish after dementia diagnosis, whereby dementia-related underlying processes in AD and FTLD may begin to merge. The Aβ1-42/Ng ratio discriminated AD from FTLD patients better than Ng alone. CSF Ng levels were not related to memory in AD or FTLD, suggesting that Ng may be a marker of the biological signs of disease state rather than cognitive deficits.

• MeSH
• Alzheimer Disease * cerebrospinal fluid   diagnosis   MeSH
• Amyloid beta-Peptides cerebrospinal fluid   MeSH
• Apolipoproteins E genetics   cerebrospinal fluid   MeSH
• Biomarkers * cerebrospinal fluid   MeSH
• Frontotemporal Lobar Degeneration * cerebrospinal fluid   diagnosis   MeSH
• Cognitive Dysfunction * cerebrospinal fluid   diagnosis   MeSH
• Middle Aged MeSH
• Humans MeSH
• Neurogranin * cerebrospinal fluid   MeSH
• Neuropsychological Tests MeSH
• Cross-Sectional Studies MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

INTRODUCTION: Loneliness has a rising public health impact, but research involving neuropathology and representative cohorts has been limited. METHODS: Inverse odds of selection weights were generalized from the autopsy sample of Rush Alzheimer's Disease Center cohorts (N = 680; 89 ± 9 years old; 25% dementia) to the US-representative Health and Retirement Study (N = 8469; 76 ± 7 years old; 5% dementia) to extend external validity. Regressions tested cross-sectional associations between loneliness and (1) Alzheimer's disease (AD) and cerebrovascular pathology; (2) five cognitive domains; and (3) relationships between pathology and cognition, adjusting for depression. RESULTS: In weighted models, greater loneliness was associated with microinfarcts, lower episodic and working memory in the absence of AD pathology, lower working memory in the absence of infarcts, a stronger association of infarcts with lower episodic memory, and a stronger association of microinfarcts with lower working and semantic memory. DISCUSSION: Loneliness may relate to AD through multiple pathways involving cerebrovascular pathology and cognitive reserve. HIGHLIGHTS: Loneliness was associated with worse cognition in five domains. Loneliness was associated with the presence of microinfarcts. Loneliness moderated cognition-neuropathology associations. Transportability methods can provide insight into selection bias.

• MeSH
• Alzheimer Disease * psychology   pathology   MeSH
• Cerebrovascular Disorders * psychology   pathology   MeSH
• Cognition * physiology   MeSH
• Humans MeSH
• Neuropsychological Tests statistics & numerical data   MeSH
• Loneliness * psychology   MeSH
• Cross-Sectional Studies MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

INTRODUCTION: In this study we assessed the contribution of psychopathology, including the two domains of negative symptoms (motivational deficit and expressive deficit), processing speed as an index of neurocognition, and emotion recognition, as an index of social cognition, to poor functional outcomes in people with schizophrenia. METHODS: The Positive and Negative Syndrome Scale was used to evaluate positive symptoms and disorganization and the Brief Negative Symptom Scale to assess negative symptoms. The Symbol Coding and the Trail Making Test A and B were used to rate processing speed and the Facial Emotion Identification Test to assess emotion recognition. Functional outcome was assessed with the Personal and Social Performance Scale (PSP). Regression analyses were performed to identify predictors of functional outcome. Mediation analyses was used to investigate whether social cognition and negative symptom domains fully or partially mediated the impact of processing speed on functional outcome. RESULTS: One hundred and fifty subjects from 8 different European centers were recruited. Our data showed that the expressive deficit predicted global functioning and together with motivational deficit fully mediated the effects of neurocognition on it. Motivational deficit was a predictor of personal and social functioning and fully mediated neurocognitive impairment effects on the same outcome. Both motivational deficit and neurocognitive impairment predicted socially useful activities, and the emotion recognition domain of social cognition partially mediated the impact of neurocognitive deficits on this outcome. CONCLUSIONS: Our results indicate that pathways to functional outcomes are specific for different domains of real-life functioning and that negative symptoms and social cognition mediate the impact of neurocognitive deficits on different domains of functioning. Our results suggest that both negative symptoms and social cognition should be targeted by psychosocial interventions to enhance the functional impact of neurocognitive remediation.

• Publication type
• Journal Article MeSH

BACKGROUND: Mild behavioral impairment (MBI) has been commonly reported in early Alzheimer's disease (AD) but rarely using biomarker-defined samples. It is also unclear whether genetic polymorphisms influence MBI in such individuals. We thus aimed to examine the association between the cognitive status of participants (amnestic mild cognitive impairment (aMCI-AD) vs cognitively normal (CN) older adults) and MBI severity. Within aMCI-AD, we further examined the association between APOE and BDNF risk genetic polymorphisms and MBI severity. METHODS: We included 62 aMCI-AD participants and 50 CN older adults from the Czech Brain Aging Study. The participants underwent neurological, comprehensive neuropsychological examination, APOE and BDNF genotyping, and magnetic resonance imaging. MBI was diagnosed with the Mild Behavioral Impairment Checklist (MBI-C), and the diagnosis was based on the MBI-C total score ≥ 7. Additionally, self-report instruments for anxiety (the Beck Anxiety Inventory) and depressive symptoms (the Geriatric Depression Scale-15) were administered. The participants were stratified based on the presence of at least one risk allele in genes for APOE (i.e., e4 carriers and non-carriers) and BDNF (i.e., Met carriers and non-carriers). We used linear regressions to examine the associations. RESULTS: MBI was present in 48.4% of the aMCI-AD individuals. Compared to the CN, aMCI-AD was associated with more affective, apathy, and impulse dyscontrol but not social inappropriateness or psychotic symptoms. Furthermore, aMCI-AD was related to more depressive but not anxiety symptoms on self-report measures. Within the aMCI-AD, there were no associations between APOE e4 and BDNF Met and MBI-C severity. However, a positive association between Met carriership and self-reported anxiety appeared. CONCLUSIONS: MBI is frequent in aMCI-AD and related to more severe affective, apathy, and impulse dyscontrol symptoms. APOE and BDNF polymorphisms were not associated with MBI severity separately; however, their combined effect warrants further investigation.

• MeSH
• Alzheimer Disease * diagnostic imaging   epidemiology   genetics   MeSH
• Apolipoproteins E genetics   MeSH
• Genotype MeSH
• Cognitive Dysfunction * diagnostic imaging   epidemiology   genetics   MeSH
• Humans MeSH
• Brain-Derived Neurotrophic Factor genetics   MeSH
• Neuropsychological Tests MeSH
• Polymorphism, Genetic genetics   MeSH
• Aged MeSH
• Check Tag
• Humans MeSH
• Aged MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH