Alzheimer's disease (AD) is a major neurodegenerative disease, affecting more than two third cases of dementia in the world. Non‑steroidal anti‑inflammatory drugs (NSAIDs) are widely used anti‑inflammatory analgesic agents representing 7.7% of worldwide prescriptions of which 90% are in patients over 65 years old. Based on mixed findings a systematic review and meta‑analysis were conducted to develop a better understanding of the protective role of NSAIDs in AD. We used three database PubMed, Web of Science, and Embase to identify the literatures. The studies following cohort and case‑control design were investigated separately to check the effect of NSAIDs on AD, by the using their fundamental indicators (relative risk and odds ratio). The fixed effect or random effects model were used to estimate the pooled relative risk and pooled odds ratio separately for both the study design, based on magnitude of heterogeneity. A total of 14 studies were selected for meta‑analysis. Eight studies were following cohort study design, whereas, six studies were following case‑control study design. In meta‑analysis of cohort studies, the pooled relative risk was 0.67 with 95% C.I 0.39 to 1.15, which was statistically insignificant. In meta‑analysis of case‑control studies, the pooled odds ratio was 0.71 with 95% C.I 0.46 to 1.10, which was statistically insignificant. NSAIDs do not act as a protective factor for Alzheimer's disease. Additionally, methodologically sound randomized controlled trials are required to produce a robust result.
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http://dx.doi.org/10.55782/ane-2023-2467 | DOI Listing |
Amino Acids
January 2025
Institute of Brain Science, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, P. R. China.
Metabolomics provide a promising tool for understanding dementia pathogenesis and identifying novel biomarkers. This study aimed to identify amino acid biomarkers for Alzheimer's Disease (AD) and Vascular Dementia (VD). By amino acid metabolomics, the concentrations of amino acids were determined in the serum of AD and VD patients as well as age-matched healthy controls.
View Article and Find Full Text PDFActa Neuropathol
January 2025
Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
Down syndrome (DS) is strongly associated with Alzheimer's disease (AD) due to APP overexpression, exhibiting Amyloid-β (Aβ) and Tau pathology similar to early-onset (EOAD) and late-onset AD (LOAD). We evaluated the Aβ plaque proteome of DS, EOAD, and LOAD using unbiased localized proteomics on post-mortem paraffin-embedded tissues from four cohorts (n = 20/group): DS (59.8 ± 4.
View Article and Find Full Text PDFJ Neurochem
January 2025
Center for Protein Diagnostics (PRODI) Biospectroscopy, Ruhr University Bochum, Bochum, Germany.
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Aβ) plaques in the brain, contributing to neurodegeneration. This study investigates lipid alterations within these plaques using a novel, label-free, multimodal approach. Combining infrared (IR) imaging, machine learning, laser microdissection (LMD), and flow injection analysis mass spectrometry (FIA-MS), we provide the first comprehensive lipidomic analysis of chemically unaltered Aβ plaques in post-mortem human AD brain tissue.
View Article and Find Full Text PDFAust N Z J Psychiatry
January 2025
Neuropsychiatry Centre, The Royal Melbourne Hospital, Parkville, VIC, Australia.
Introduction: Young-onset neurocognitive symptoms result from a heterogeneous group of neurological and psychiatric disorders which present a diagnostic challenge. To identify such factors, we analysed the Biomarkers in Younger-Onset Neurocognitive Disorders cohort, a study of individuals <65 years old presenting with neurocognitive symptoms for a diagnosis and who have undergone cognitive and biomarker analyses.
Methods: Sixty-five participants (median age at assessment of 56 years, 45% female) were recruited during their index presentation to the Royal Melbourne Hospital Neuropsychiatry Centre, a tertiary specialist service in Melbourne, Australia, and categorized as either early-onset Alzheimer's disease ( = 18), non-Alzheimer's disease neurodegeneration ( = 23) or primary psychiatric disorders ( = 24).
Alzheimers Res Ther
January 2025
Department of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0948, USA.
Background: Effective detection of cognitive impairment in the primary care setting is limited by lack of time and specialized expertise to conduct detailed objective cognitive testing and few well-validated cognitive screening instruments that can be administered and evaluated quickly without expert supervision. We therefore developed a model cognitive screening program to provide relatively brief, objective assessment of a geriatric patient's memory and other cognitive abilities in cases where the primary care physician suspects but is unsure of the presence of a deficit.
Methods: Referred patients were tested during a 40-min session by a psychometrist or trained nurse in the clinic on a brief battery of neuropsychological tests that assessed multiple cognitive domains.
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