The aim of this study was to evaluate the levels of anti-GM1 in demented patients, correlating them with the type and severity of dementia as well as with the eventually coexistent polyneuropathy. Anti-GM1 concentrations were measured in the sera of 33 demented patients with a male-to-female ratio of 1:2.7 (the mean age was 69.7 years for males and 70.1 years for females). Eighty-two percent of the patients revealed increased values of anti-GM1, but only 18.2% demonstrated polyneuropathies. Fifty-nine percent of the patients suffered from vascular dementia. The most severely demented patients demonstrated a Mini-Mental State Examination score of 5 to 23 out of 30 and revealed the most increased levels of anti-GM1 (>40 EU/mL). The findings of this study are indicative of a possible correlation between the levels of anti-GM1 and the severity of dementia, mainly of the vascular type.
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http://dx.doi.org/10.1177/1533317508317816 | DOI Listing |
Alzheimers Dement
January 2025
Unitat de Trastorns Cognitius, Cognition and Behavior Study Group, Hospital Universitari Santa Maria Universitat de Lleida, Lleida, Spain.
Introduction: Changes in sleep physiology can predate cognitive symptoms by decades in persons with Alzheimer's disease (AD), but it remains unclear which sleep characteristics predict cognitive and neurodegenerative changes after AD onset.
Methods: Using data from a prospective cohort of mild to moderate AD (n = 60), we analyzed non-rapid eye movement sleep spindles and slow oscillations (SOs) at baseline and their associations with baseline amyloid beta (Aβ) and tau and with cognition from baseline to 3-year follow-up.
Results: Higher spindle and SO activity predicted significant changes in Aβ and tau at baseline, lower Alzheimer's Disease Assessment Scale Cognitive Subscale (better cognitive performance) score, and higher Mini-Mental State Examination score from baseline to 36 months.
Alzheimers Dement
January 2025
Department of Radiology, China-Japan Friendship Hospital, Beijing, China.
Introduction: The link between overload brain iron and transcriptional/cellular signatures in Alzheimer's disease (AD) remains inconclusive.
Methods: Iron deposition in 41 cortical and subcortical regions of 30 AD patients and 26 healthy controls (HCs) was measured using quantitative susceptibility mapping (QSM). The expression of 15,633 genes was estimated in the same regions using transcriptomic data from the Allen Human Brain Atlas (AHBA).
Alzheimers Dement
January 2025
Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Xicheng District, Beijing, China.
Alzheimer's disease (AD) is a degenerative disease characterized by progressive cognitive dysfunction. The strong link between nutrition and the occurrence and progression of AD pathology has been well documented. Poor nutritional status accelerates AD progress by potentially aggravating amyloid beta (Aβ) and tau deposition, exacerbating oxidative stress response, modulating the microbiota-gut-brain axis, and disrupting blood-brain barrier function.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Laboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium.
Introduction: The automated analysis of connected speech using natural language processing (NLP) emerges as a possible biomarker for Alzheimer's disease (AD). However, it remains unclear which types of connected speech are most sensitive and specific for the detection of AD.
Methods: We applied a language model to automatically transcribed connected speech from 114 Flemish-speaking individuals to first distinguish early AD patients from amyloid negative cognitively unimpaired (CU) and then amyloid negative from amyloid positive CU individuals using five different types of connected speech.
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.
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