Background: Apathy is a neuropsychiatric symptom frequently observed in patients with cognitive impairment. It has been found to be a predictor of conversion from mild cognitive impairment (MCI) to dementia of Alzheimer disease type. However, this association between apathy and dementia conversion has not yet been confirmed in vascular MCI, especially post-stroke MCI. The aim of this study was to evaluate whether apathy would increase the risk of dementia conversion in patients with post-stroke MCI after 6 months.
Method: A prospective multi-centre cohort study was performed in 14 clinics in seven provinces and cities of China. A total of 989 subjects were included 2 weeks to 6 months after stroke, and met the diagnostic criteria of International Working Group for MCI. Symptoms of apathy were assessed using the apathy subscale of Geriatric Depression Scale. Subjects were divided into an apathy group (n = 128) and a non-apathy group (n = 861). The primary outcome was the dementia conversion after 6 months. To eliminate potential biases, subjects were chosen from 861 non-apathy patients with similarity in seven potential predictors of cognitive impairment to match with the apathy group (n = 128) at a 1:1 ratio, as a matched non-apathy group (n = 128). The dementia conversion rate was compared between the apathy group (n = 128) and its correspondingly matched non-apathy group (n = 128), and the relative risk (RR) was calculated.
Results: The prevalence of apathy in post-stroke MCI was 12.9%. After 6 months, 5.2% of patients with post-stroke MCI converted to dementia. The dementia conversion rate of the apathy group was significantly higher than that of the non-apathy group before case-matching (17.2% vs 3.4%, P < 0.001), and also after case-matching (17.2% vs 6.3%, P < 0.001). Symptoms of apathy increased the risk of conversion from MCI to dementia (RR 2.75, 95% CI 1.272-5.947, P < 0.001).
Conclusions: For patients with post-stroke MCI, apathy symptoms increase the risk of conversion from MCI to dementia.
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http://dx.doi.org/10.1111/psyg.12634 | DOI Listing |
Alzheimers Dement
January 2025
Department of Psychiatry and Neuroscience, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.
Introduction: The beneficial effects of amyloid beta 1-38, or Aβ(1-38), on Alzheimer's disease (AD) progression in humans in vivo remain controversial. We investigated AD patients' cerebrospinal fluid (CSF) Aβ(1-38) and AD progression.
Methods: Cognitive function and diagnostic change were assessed annually for 3 years in 177 Aβ-positive participants with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and dementia from the German Center for Neurodegenerative Diseases (DZNE) longitudinal cognitive impairment and dementia study (DELCODE) cohort using the Mini-Mental State Examination (MMSE), Preclinical Alzheimer's Cognitive Composite (PACC), Clinical Dementia Rating (CDR), and National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria.
Introduction: Artificial intelligence and neuroimaging enable accurate dementia prediction, but 'black box' models can be difficult to trust. Explainable artificial intelligence (XAI) describes techniques to understand model behaviour and the influence of features, however deciding which method is most appropriate is non-trivial. Vision transformers (ViT) have also gained popularity, providing a self-explainable, alternative to traditional convolutional neural networks (CNN).
View Article and Find Full Text PDFJ Prev Alzheimers Dis
February 2025
The ADNI is detailed in Supplemental Acknowledgments.
Background: α-Synuclein (α-Syn) pathology is present in 30-50 % of Alzheimer's disease (AD) patients, and its interactions with tau proteins may further exacerbate pathological changes in AD. However, the specific role of different aggregation forms of α-Syn in the progression of AD remains unclear.
Objectives: To explore the relationship between various aggregation types of CSF α-Syn and Alzheimer's disease progression.
J Integr Neurosci
January 2025
Department of Radiology, Affiliated Hospital of North Sichuan Medical College, 637000 Nanchong, Sichuan, China.
Background: Volume alterations in the parietal subregion have received less attention in Alzheimer's disease (AD), and their role in predicting conversion of mild cognitive impairment (MCI) to AD and cognitively normal (CN) to MCI remains unclear. In this study, we aimed to assess the volumetric variation of the parietal subregion at different cognitive stages in AD and to determine the role of parietal subregions in CN and MCI conversion.
Methods: We included 662 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, including 228 CN, 221 early MCI (EMCI), 112 late MCI (LMCI), and 101 AD participants.
Medicina (Kaunas)
January 2025
Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul 06351, Republic of Korea.
: While depression is associated with an increased risk of Alzheimer's dementia (AD), traditional AD-related biomarkers, such as amyloid-beta, have shown limited predictive value for late-life depression. Oxidative stress has emerged as a potential indicator given its shared role in both depression and dementia. This study investigated the longitudinal relationship between oxidative stress biomarkers and risk of dementia in patients with depression.
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