Background: Alzheimer's disease (AD) is the leading cause of dementia. Currently, no definitive diagnostic test for AD exists. Cerebrospinal fluid (CSF) concentrations of amyloid beta (Abeta1-42) peptides and total tau proteins (T-tau) may serve as biomarkers for AD.
Aim: The objective of this study was to investigate the usefulness of CSF Abeta1-42 and T-tau analyses in the diagnosis of AD with Tunisians.
Methods: We focused on three groups originating from Central Tunisian that matched in age (range 48-85): healthy controls (n = 53), AD patients (n = 93) and non-Alzheimer (nAD) dementia (n = 35) patients. Abeta1-42 and T-tau levels were measured in CSF by sandwich enzyme-linked immunosorbent assay.
Results: The ratio of T-tau/Abeta1-42 at baseline yielded a sensitivity of 85.3% for detection of AD and the specificity was 84.8% to differentiate controls and nAD dementia.
Conclusion: Our findings confirm the use of T-tau/Abeta1-42 ratio in the discrimination of AD patients from all other patients.
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http://dx.doi.org/10.1159/000241881 | DOI Listing |
Alzheimers Dement
December 2024
1st Department of Neurology, Aiginition Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Background: Numerous studies have highlighted the role of oxidative stress in Alzheimer's disease (AD) development. Yet, the alignment of systemic and central oxidative stress biomarkers is unclear across diverse populations in the AD continuum. This study aims to assess protein damage levels in plasma and cerebrospinal fluid (CSF) within the AD continuum.
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December 2024
The Second Affiliated Hospital of Chongqing Medical University, Chongqing, Chong Qing, China.
Background: Alzheimer's disease (AD) frequently coexists with cerebral small vessel disease (CSVD) is common in the aging population, yet the underlying mechanisms are not yet fully understood. Both long-term blood pressure variability (BPV) and plasma neurofilament light (PNFL) were identified as potential biomarkers for AD and CSVD. This study aims to understand the mechanisms of comorbidity between AD and CSVD by investigating the associations among BPV, PNFL, and comorbidity.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Background: The brain is shielded from the peripheral circulation by central nervous system (CNS) barriers, comprising the well-known blood-brain barrier (BBB) and the less recognized blood-cerebrospinal fluid (CSF) barrier located within the brain ventricles. The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host, including the development of neurological disorders like Alzheimer's disease (AD). However, the intricate mechanisms governing the interplay between the gut and brain remain elusive, and the means by which gut-derived signals traverse the CNS barriers remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Queen's University, Kingston, ON, Canada; D'OR Institute for Research and Education, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Physical exercise improves overall brain health, cognition, and stimulates the release of extracellular vesicles (EVs) in humans. Exercise upregulates irisin, a myokine derived from fibronectin type III domain-containing protein 5 (FNDC5) previously shown to mediate the beneficial actions of exercise on memory in mouse models of Alzheimer's disease (AD). Here, we investigated if physical exercise upregulates EVs.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Radiology, miami, FL, USA.
Background: Clearance of brain toxins occurs during sleep, although the mechanism remains unknown. Previous studies implied that the intracranial aqueductal cerebrospinal fluid (CSF) oscillations are involved, but no mechanism was suggested. The rationale for focusing on the aqueductal CSF oscillations is unclear.
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