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Abnormal synaptic plasticity leads to cognitive impairment in schizophrenia. Markers of synaptic plasticity are known to be altered in schizophrenia, but there are limited data available about neural cell adhesion molecule-1 (NCAM-1) levels and its association with cognitive functions in schizophrenia. The objective of the study was to analyze NCAM-1 levels and its association with various cognitive domains in schizophrenia. One hundred and seventy-six schizophrenia cases and 176 controls were recruited for the study. Serum NCAM-1 levels were analysed in both the groups. Cognitive examination was performed using Addenbrooke cognitive examination-III (ACE-III) and disease severity was assessed using Positive and negative symptoms scale (PANSS). Serum NCAM-1 levels were elevated in schizophrenia cases ( = 0.006) compared to controls. NCAM-1 was positively associated with attention (r = 0.196, = 0.009), language (r = 0.192, = 0.011), visuospatial abilities (r = 0.207, p = 0.006) and total ACE-III score (r = 0.189, = 0.012). We conclude that elevated levels of NCAM-1 are associated with better cognitive functioning in schizophrenia.
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http://dx.doi.org/10.1007/s12291-020-00937-y | DOI Listing |
BackgroundAlzheimer's disease (AD), a neurodegenerative condition and major subtype of dementia, is often preceded by mild cognitive impairment (MCI), a transitional stage before dementia. While cerebrospinal fluid (CSF) biomarkers are widely used for diagnosing AD and MCI, blood-based biomarkers offer the advantage of easier accessibility. This study aimed to compare blood levels of nine biomarkers among healthy controls, patients with MCI, and those with dementia, and to evaluate their potential for predicting AD progression.
View Article and Find Full Text PDFNat Commun
April 2025
Centre for Discovery Brain Sciences, The University of Edinburgh, Edinburgh, UK.
In Alzheimer's disease, amyloid beta (Aβ) and tau pathology are thought to drive synapse loss. However, there is limited information on how endogenous levels of tau, Aβ and other biomarkers relate to patient characteristics, or how manipulating physiological levels of Aβ impacts synapses in living adult human brain. Using live human brain slice cultures, we report that Aβ and tau release levels vary with donor age and brain region, respectively.
View Article and Find Full Text PDFBiochemistry (Mosc)
February 2025
Research Center of Neurology, Moscow, 125367, Russia.
Amyotrophic lateral sclerosis (ALS) is the most prevalent motor neuron disease. However, definitive diagnosis could be delayed by up to 12 months due to the lack of specific and sensitive biomarkers for ALS. In our study, conducted for the first time on a large cohort of ALS patients ( = 100) within the Russian population, we assessed key biomarkers of neurodegenerative pathology, including β-amyloids (Aβ40 and Aβ42) and tau proteins (Tau-total and Tau-p181), as well as other pathogenetically relevant, promising biomarkers such as FGF-21, Kallikrein-6 (KLK-6), NCAM-1, Neurogranin (NRGN), TDP-43, Apolipoprotein E4, Clusterin (Apo J), Complement Factor H, Fetuin-A, α2-Macroglobulin, Apo AI, Apo CIII, Apo E, Complement C3, GDNF, sRAGE, and S100B protein.
View Article and Find Full Text PDFJ Infect Dis
June 2025
Department of Infection Biology, London School of Hygiene and Tropical Medicine, United Kingdom.
Background: Malaria remains a major public health concern with substantial morbidity and mortality worldwide. In Malaysia, the emergence of Plasmodium knowlesi has led to a surge in zoonotic malaria cases and deaths in recent years. Signs of cerebral involvement have been observed in a noncomatose, fatal case of knowlesi infection, but the potential impact of this malaria species on the brain remains unexplored.
View Article and Find Full Text PDFMetab Brain Dis
November 2024
Departamento de Análises Clínicas, Faculdade de Farmácia, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Propionic and methylmalonic acidemias (PAcidemia and MMAcidemia, respectively) are genetic disorders characterized by acute metabolic decompensation and neurological complications. L-carnitine (LC) is effective in reducing toxic metabolites that are related to the pathophysiology of these diseases. Therefore we investigated biomarkers of inflammation (cytokines and C-reactive protein (CRP)), neurodegeneration (BDNF, NCAM-1 and cathepsin-D) and biomolecules oxidation (sulfhydryl content and thiobarbituric acid-reactive species (TBARS)), as well as carnitine concentrations in untreated patients with PAcidemia and MMAcidemia, in patients under treatment with LC and a protein-restricted diet for until 2 years and in patients under the same treatment for more than 2 years.
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