Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring最新文献

{"title":"Acoustic speech features are associated with late-life depression and apathy symptoms: Preliminary findings.","authors":"Daniel Harlev, Shir Singer, Maya Goldshalger, Noham Wolpe, Eyal Bergmann","doi":"10.1002/dad2.70055","DOIUrl":"10.1002/dad2.70055","url":null,"abstract":"<p><strong>Background: </strong>Late-life depression (LLD) is a heterogenous disorder related to cognitive decline and neurodegenerative processes, raising a need for the development of novel biomarkers. We sought to provide preliminary evidence for acoustic speech signatures sensitive to LLD and their relationship to depressive dimensions.</p><p><strong>Methods: </strong>Forty patients (24 female, aged 65-82 years) were assessed with the Geriatric Depression Scale (GDS). Vocal features were extracted from speech samples (reading a pre-written text) and tested as classifiers of LLD using random forest and XGBoost models. Post hoc analyses examined the relationship between these acoustic features and specific depressive dimensions.</p><p><strong>Results: </strong>The classification models demonstrated moderate discriminative ability for LLD with receiver operating characteristic = 0.78 for random forest and 0.84 for XGBoost in an out-of-sample testing set. The top classifying features were most strongly associated with the apathy dimension (<i>R</i> ² = 0.43).</p><p><strong>Discussion: </strong>Acoustic vocal features that may support the diagnosis of LLD are preferentially associated with apathy.</p><p><strong>Highlights: </strong>The depressive dimensions in late-life depression (LLD) have different cognitive correlates, with apathy characterized by more pronounced cognitive impairment.Acoustic speech features can predict LLD. Using acoustic features, we were able to train a random forest model to predict LLD in a held-out sample.Acoustic speech features that predict LLD are preferentially associated with apathy. These results indicate a predominance of apathy in the vocal signatures of LLD, and suggest that the clinical heterogeneity of LLD should be considered in development of acoustic markers.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70055"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between choroidal microvasculature in the eye and Alzheimer's disease risk in cognitively healthy mid-life adults: A pilot study.","authors":"Jamie Burke, Samuel Gibbon, Audrey Low, Charlene Hamid, Megan Reid-Schachter, Graciela Muniz-Terrera, Craig W Ritchie, Baljean Dhillon, John T O'Brien, Stuart King, Ian J C MacCormick, Thomas J MacGillivray","doi":"10.1002/dad2.70075","DOIUrl":"10.1002/dad2.70075","url":null,"abstract":"<p><strong>Introduction: </strong>We explored associations between measurements of the ocular choroid microvasculature and Alzheimer's disease (AD) risk.</p><p><strong>Methods: </strong>We measured the choroidal vasculature appearing in optical coherence tomography (OCT) scans of 69 healthy, mid-life individuals in the PREVENT Dementia cohort. The cohort was prospectively split into low-, medium-, and high-risk groups based on the presence of known risk factors (apolipoprotein E [<i>APOE</i>] ε4 genotype and family history of dementia [FH]). We used ordinal logistic regression to test for cross-sectional associations between choroidal measurements and AD risk.</p><p><strong>Results: </strong>Choroidal vasculature was progressively larger between ordinal risk groups, and significantly associated with risk group prediction. <i>APOE</i> ε4 carriers had thicker choroids and larger vascularity compared to non-carriers. Similar trends were observed for those with a FH.</p><p><strong>Discussions: </strong>Our results suggest a potential link between the choroidal vasculature and AD risk. However, these exploratory findings should be replicated in a larger sample.</p><p><strong>Highlights: </strong>Ocular choroidal microvasculature is of interest in relation to neurodegeneration due to its autonomic response to systemic, pathophysiological change.Choroidal changes in the prodromal stage of Alzheimer's disease (AD) are unexplored.The PREVENT Dementia cohort offers a unique, non-invasive study of the microvasculature in mid-life individuals at increased risk for developing AD.Significantly increased ocular choroidal vasculature was associated with increased risk (apolipoprotein E carrier and/or family history of dementia) for AD.These exploratory results suggest a potential association between the ocular choroidal vasculature and AD risk. However, findings should be replicated in a larger sample.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70075"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A longitudinal study of functional brain complexity in progressive Alzheimer's disease.","authors":"Ru Zhang, Leon Aksman, Dilmini Wijesinghe, John M Ringman, Danny J J Wang, Kay Jann","doi":"10.1002/dad2.70059","DOIUrl":"10.1002/dad2.70059","url":null,"abstract":"<p><strong>Introduction: </strong>Cross-sectional resting-state functional magnetic resonance imaging (rsfMRI) studies have revealed altered complexity with advanced Alzheimer's disease (AD) stages. The current study conducted longitudinal rsfMRI complexity analyses in AD.</p><p><strong>Methods: </strong>Linear mixed-effects (LME) models were implemented to evaluate altered rates of disease progression in complexity across disease groups.</p><p><strong>Results: </strong>The LME models revealed complexity of the higher frequency in the CNtoMCI group (those converted from cognitively normal [CN] to mild cognitive impairment [MCI]) decayed faster over time versus CN in the prefrontal and lateral occipital cortex; complexity of the lower frequency decayed faster in AD versus CN in various frontal and temporal regions (<i>p</i> < 0.05 & Benjamini-Hochberg corrected with <i>q</i> < 0.05).</p><p><strong>Discussion: </strong>Local functional brain activities decayed in the early stage of the disease, and long-range communications were impacted in the later stage. Our study demonstrated longitudinal changes in AD-related rsfMRI complexity, indicating its potential as an imaging biomarker of AD.</p><p><strong>Highlights: </strong>We conducted longitudinal resting state functional magnetic resonance imaging (rsfMRI) complexity analyses using the Alzheimer's Disease Neuroimaging Initiative dataset.Higher-frequency complexity in the CNtoMCI group (those transitioning from cognitively normal [CN] to mild cognitive impairment [MCI]) was found to decay faster over time compared to CN, specifically in the prefrontal and lateral occipital cortex.Lower-frequency complexity was found to decay faster in AD versus CN in various frontal and temporal regions.This study demonstrated that longitudinal changes in rsfMRI complexity could serve as a potential imaging biomarker for Alzheimer's disease.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70059"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the relationship between melanopsin gene variants, sleep, and markers of brain health.","authors":"Ayeisha Milligan Armstrong, Eleanor O'Brien, Tenielle Porter, Vincent Dore, Pierrick Bourgeat, Paul Maruff, Christopher C Rowe, Victor L Villemagne, Stephanie R Rainey-Smith, Simon M Laws","doi":"10.1002/dad2.70056","DOIUrl":"10.1002/dad2.70056","url":null,"abstract":"<p><strong>Introduction: </strong>Melanopsin is a photopigment with roles in mediating sleep and circadian-related processes, which are often disrupted in Alzheimer's disease (AD). Melanopsin also impacts cognition and synaptogenesis. This study investigated the associations between melanopsin genetic variants, sleep, and markers of brain health.</p><p><strong>Methods: </strong>Linear regression analyses examined the relationship of single-nucleotide polymorphisms (SNPs) within the melanopsin gene (<i>OPN4</i>), with cortical amyloid beta (Aβ), cognition, brain volumes, and self-reported sleep traits in cognitively unimpaired older adults. Further analyses assessed whether sleep traits x <i>OPN4</i> SNP interactions were associated with markers of brain health.</p><p><strong>Results: </strong><i>OPN4</i> SNPs rs2355009 and rs3740334 were associated with attention and processing speed and ventricular volume and language, respectively. Furthermore, rs3740334 and rs1079610 showed significant interactions with sleep traits in association with language.</p><p><strong>Discussion: </strong>This study shows associations of <i>OPN4</i> genetic variants with markers of brain health, and suggests that these variants interact with sleep to exacerbate cognitive effects.</p><p><strong>Highlights: </strong>The relationships between melanopsin gene (<i>OPN4</i>) variants and markers of brain health were examined cross-sectionally in cognitively unimpaired older individuals.Variation within <i>OPN4</i>is associated with differences in cognition and ventricular volume.rs2355009 and rs3740334 show small-moderate associations with differences in attention and processing speed. Further to this, rs2355009 and rs3740334 were associated with ventricular volumes and language performance, respectively.The interactions between rs3740334 and rs1079610 and sleep traits also showed small-moderate associations with differences in language performance.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70056"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"sTREM2 in discordant CSF Aβ₄₂ and p-tau181.","authors":"Danni Li, William G Mantyh, Lu Men, Ishika Jain, Matthew Glittenberg, Binchong An, Lin Zhang, Ling Li","doi":"10.1002/dad2.70072","DOIUrl":"10.1002/dad2.70072","url":null,"abstract":"<p><strong>Introduction: </strong>Little is known about the factors underpinning discordant cerebrospinal fluid (CSF) amyloid beta (Aβ)₄₂ versus p-tau181/Aβ₄₂ or CSF Aβ₄₂ versus Aβ positron emission tomography (PET).</p><p><strong>Methods: </strong>We stratified 570 non-demented Alzheimer's Disease Neuroimaging Initiative (ADNI) participants by Aβ PET and further by CSF Aβ₄₂ or p-tau181/Aβ₄₂. We used analysis of covariance testing adjusting for covariates, followed by Tukey post hoc pairwise comparisons, to compare CSF soluble triggering receptor expressed on myeloid cells-2 (sTREM2) across four participant groups: CSF+ _Aβ42 with CSF- _p-tau/Aβ42, CSF- _Aβ42 with CSF+ _p-tau/Aβ42, and concordant CSF_Aβ42/CSF_p-tau/Aβ42. We also compared sTREM2 across discordant and concordant CSF_Aβ42/PET.</p><p><strong>Results: </strong>Regardless of Aβ PET status, CSF+_Aβ42 with CSF-_p-tau/Aβ42 had lower sTREM2 than CSF-_Aβ42 with CSF+_p-tau/Aβ42. CSF sTREM2 was similarly also associated with discordant CSF Aβ42 /PET.</p><p><strong>Discussion: </strong>Our study suggests the potential roles of sTREM2 in discordant CSF Aβ₄₂ and p-tau181/Aβ₄₂ and discordant CSF_Aβ42/PET. Low- and high-CSF sTREM2 may affect the accuracy of p-tau181/Aβ₄₂ during the clinical work-up of AD.</p><p><strong>Highlights: </strong>17% of non-demented older adults had discordant CSF Aβ₄₂ versus p-tau181/Aβ₄₂.sTREM2 differed between discordant cases of CSF Aβ₄₂ versus p-tau181/Aβ₄₂.20% of non-demented older adults had discordant CSF Aβ₄₂ versus Aβ PET.sTREM2 also differed between discordant cases of CSF Aβ₄₂ versus Aβ PET.p-tau181/Aβ₄₂ may miss 6.7% of PET+ non-demented older adults with low sTREM2.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70072"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward alpha-synuclein seed amplification assay in clinical practice.","authors":"Mathieu Verdurand, Flora Kaczorowski, Sophie Dautricourt, Virginie Desestret, Maïté Formaglio, Hélène Mollion, Gil Petitnicolas, Ali Afifi, Anthony Fourier, Antoine Garnier-Crussard, Isabelle Quadrio","doi":"10.1002/dad2.70066","DOIUrl":"10.1002/dad2.70066","url":null,"abstract":"<p><strong>Introduction: </strong>Seed amplification assays (SAAs) demonstrate remarkable diagnostic performance in alpha-synucleinopathies. However, existing protocols lack accessibility in routine laboratories, mainly due to the requirement for in-house production of recombinant alpha-synuclein (aSyn). This study proposes a cerebrospinal fluid (CSF) aSyn-SAA protocol using solely commercial reagents to facilitate its clinical implementation.</p><p><strong>Methods: </strong>Routine clinical care CSF samples from 126 patients, comprising 47 with Lewy body diseases (LBD) (41 with dementia with Lewy bodies, six with Parkinson's disease), 37 without alpha-synucleinopathy, and 42 with Alzheimer's disease (AD), underwent assessment for aSyn-SAA activity.</p><p><strong>Results: </strong>CSF aSyn-SAA showed a sensitivity of 72.3% and a specificity of 100% when distinguishing clinically diagnosed LBD patients from those without alpha-synucleinopathy. In AD patients, 14.3% were tested positive for aSyn.</p><p><strong>Discussion: </strong>The commercial-only CSF aSyn-SAA protocol exhibited excellent specificity when applied to a real-life cohort, signaling progress toward the accessibility of an aSyn biomarker in clinical settings.</p><p><strong>Highlights: </strong>Diagnosis of LBD through aSyn-SAA lacks accessibility.This commercial-only aSyn-SAA has satisfactory performance in a real-life cohort.A negative aSyn-SAA does not completely exclude a synucleinopathy.Some technical points must be considered when developing aSyn-SAA.aSyn-SAA must be confined to expert laboratories due to prion-like risk management.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70066"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid-related changes in fluency in patients with subjective cognitive decline.","authors":"Rosanne L van den Berg, Elke Butterbrod, Casper de Boer, Lisa-Marie Schlüter, Argonde C van Harten, Charlotte E Teunissen, Elsmarieke van de Giessen, Wiesje M van der Flier, Sietske A M Sikkes","doi":"10.1002/dad2.70063","DOIUrl":"10.1002/dad2.70063","url":null,"abstract":"<p><strong>Introduction: </strong>We examined semantic and phonemic fluency in individuals with subjective cognitive decline (SCD) in relation to amyloid status and clinical progression.</p><p><strong>Methods: </strong>A total of 490 individuals with SCD (62 ± 8 years, 42% female, 28% amyloid-positive, 17% clinical progression) completed annual fluency assessments (mean ± SD follow-up 4.3 ± 2.9 years). Associations between fluency trajectories, amyloid status, and clinical progression were examined with linear mixed models and joint models.</p><p><strong>Results: </strong>Amyloid-positive individuals declined faster than amyloid-negative individuals on semantic fluency (<i>B</i> = -0.35, <i>p</i> < 0.001), but not on phonemic fluency (<i>B</i> = -0.06, <i>p</i> = 0.218). An annual decline of one word in semantic and phonemic fluency was associated with 22% (hazard ratio [HR] = 1.22, <i>p</i> < 0.001) and 28% (HR = 1.28, <i>p</i> = 0.004) increased risk of clinical progression.</p><p><strong>Discussion: </strong>Our results indicate that decline in semantic fluency is an early indicator of cognitive deficits in preclinical Alzheimer's disease.</p><p><strong>Highlights: </strong>Abnormal amyloid burden is associated with decline in semantic fluency.Fluency trajectories are associated with an increased risk of clinical progression.More refined measures are needed to detect the earliest language deficits.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70063"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical decision points for two plasma p-tau217 laboratory developed tests in neuropathology confirmed samples.","authors":"Anna E Mammel, Ging-Yuek Robin Hsiung, Ali Mousavi, Kelsey Hallett, Ian R Mackenzie, Veronica Hirsch-Reinshagen, Don Biehl, Pradip Gill, Mary Encarnacion, Hans Frykman","doi":"10.1002/dad2.70070","DOIUrl":"10.1002/dad2.70070","url":null,"abstract":"<p><strong>Introduction: </strong>We evaluated the diagnostic performance of two commercial plasma p-tau217 immunoassays compared to cerebrospinal fluid (CSF) testing and neuropathology.</p><p><strong>Methods: </strong>One hundred and seventy plasma samples from the University of British Columbia Hospital Clinic for Alzheimer's (AD) and Related Disorders were analyzed for p-tau217 using Fujirebio and ALZpath assays. Decision points were determined using CSF testing and autopsy findings as the standard.</p><p><strong>Results: </strong>Fujirebio and ALZpath p-tau217 had similar overall analytical and clinical performance, with distinct decision points for each assay. Based on autopsy findings, both p-tau217 assays identified individuals with AD from other neurodegenerative diseases (ALZpath area under the curve [AUC] = 0.94, Fujirebio AUC = 0.90). The ALZpath assay detected AD pathology at milder disease stages compared to the Fujirebio assay.</p><p><strong>Discussion: </strong>Our study reinforces the clinical utility of plasma p-tau217 as an AD biomarker. Differences in test performance and clinical decision points suggest an assay-specific diagnostic approach is required for plasma p-tau217 in clinical practice.</p><p><strong>Highlights: </strong>Two commercially available p-tau217 immunoassays (ALZpath and Fujirebio) showed equal performance based on CSF testing.ALZpath p-tau217 showed higher performance compared to Fujirebio p-tau217 based on AD diagnosis by neuropathology confirmation.Specific plasma p-tau217 assays may require distinct decision points for AD screening, diagnosis, and disease progression monitoring.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70070"},"PeriodicalIF":4.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel method for objective quantification of apathy based on gaze and physiological reactivity to stimuli presented in a virtual reality environment.","authors":"Ramit Ravona-Springer, Or Koren, Noam Galor, Michal Lapid, Yotam Bahat, Ronen Fluss, Meytal Wilf, Shlomit Zorani, Uri Rosenblum, Michal Schnaider Beeri, Meir Plotnik","doi":"10.1002/dad2.70020","DOIUrl":"10.1002/dad2.70020","url":null,"abstract":"<p><strong>Introduction: </strong>We developed a tool for objective quantification of apathy.</p><p><strong>Methods: </strong>Participants (<i>n</i> = 97; 67 with cognitive impairment, 30 cognitively normal; mean age = 74.3 ± 6.2 years, 56.7% females) were exposed to emotional and cognitive stimuli in a virtual reality environment. Gaze metrics (time to first fixation [TTFF] and total fixation duration [TFD]) and autonomic nervous system (ANS) reactivity were measured. Apathy and depression were clinically assessed using the Lille Apathy Rating Scale short version and the Geriatric Depression Scale 15-item version, respectively. Cutoffs of ≥ -7 and ≥ 5 were used to define apathy and depression, respectively.</p><p><strong>Results: </strong>The sample comprised 14 participants with apathy only, 9 with depression only, 10 with both, 63 with neither, and 1 with missing data. For all emotional stimuli, participants with apathy only showed longer TTFF (<i>P</i> = 0.039, effect sizes [ES] = 0.798), and shorter TFD (<i>P</i> = 0.023, ES = 0.578) compared to those without apathy or depression. ANS reactivity was not associated with apathy.</p><p><strong>Discussion: </strong>Apathy is associated with decreased gaze engagement at emotional stimuli.</p><p><strong>Highlights: </strong>Apathy measurement via questionnaires is limited by subjectivity biases.Apathy measurement via questionnaires is limited by simplistic scoring.We present a novel method for objective measurement of apathy.Gaze characteristics reflect the emotional and cognitive components of apathy.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70020"},"PeriodicalIF":4.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11886987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modifiable risk factors and symptom progression in dementia over up to 8 years-Results of the DelpHi-MV trial.","authors":"Iris Blotenberg, Felix Wittström, Bernhard Michalowsky, Moritz Platen, Diana Wucherer, Stefan Teipel, Wolfgang Hoffmann, Jochen René Thyrian","doi":"10.1002/dad2.70050","DOIUrl":"10.1002/dad2.70050","url":null,"abstract":"<p><strong>Introduction: </strong>This study investigated the association between modifiable factors and symptom progression in dementia over up to 8 years.</p><p><strong>Methods: </strong>Multilevel growth curve models assessed the role of modifiable risk factors (low education, hearing impairment and its treatment, depression, physical inactivity, diabetes and its treatment, smoking, hypertension and its treatment, obesity, alcohol consumption, social isolation, and visual impairment) on cognitive and functional trajectories in 353 people with dementia.</p><p><strong>Results: </strong>Higher education was associated with higher initial cognitive status but faster decline. Antidiabetic medication was associated with slower cognitive decline, whereas depression and visual impairment were linked to low baseline functioning and faster cognitive decline.</p><p><strong>Discussion: </strong>Several modifiable risk factors influenced symptom progression. Education initially had a protective effect, whereas depressive symptoms were linked to worse symptom progression. Treatment of comorbidities (diabetes, visual impairment) could have a positive impact on dementia symptoms. Modifiable risk factors are promising targets for tertiary prevention.</p><p><strong>Highlights: </strong>Modifiable risk factors were associated with symptom progression in dementia over up to 8 years.More education was associated with higher initial cognitive status but faster decline.Depressive symptoms were linked to less favorable symptom progression.Treatment of comorbidities (diabetes, visual impairment) may positively impact the course of symptoms.Modifiable risk factors are promising targets for tertiary prevention.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 1","pages":"e70050"},"PeriodicalIF":4.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}