Background: The aim of this study was to explore the relationship between cerebrospinal fluid Alzheimer's disease (AD) markers and depression in elderly people.
Method: We included subjects with AD as well as persons with subjective cognitive impairment and normal cognition. Depression was assessed with the Cornell Scale for Depression in Dementia, and a cut-off score of >6 was used to define depression. Cerebrospinal fluid was analyzed using commercially available assays for β-amyloid 1-42, total tau, and phosphorylated tau 181.
Results: A total of 183 participants (66.7% female) were included (92 with AD and 91 with subjective cognitive impairment), with a mean age (±SD) of 67.6 ± 7.4 years, a Mini-Mental State Examination score of 26.0 ± 4.0, and a median Cornell Scale for Depression in Dementia score of 5 (range 0-19). Depression scores were not associated with higher phosphorylated tau 181 and total tau or reduced β-amyloid 1-42 in AD or non-demented subjects.
Conclusions: These results suggest that AD pathology does not contribute to depression, indicating that other factors may be more important. Further studies of the aetiology of depression in elderly people with and without AD are warranted.
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http://dx.doi.org/10.1159/000334644 | DOI Listing |
J Integr Neurosci
January 2025
Department of Ophthalmology, University Hospital of Udine, 33100 Udine, Italy.
The complicated neurological syndrome known as multiple sclerosis (MS) is typified by demyelination, inflammation, and neurodegeneration in the central nervous system (CNS). Managing this crippling illness requires an understanding of the complex interactions between neurophysiological systems, diagnostic techniques, and therapeutic methods. A complex series of processes, including immunological dysregulation, inflammation, and neurodegeneration, are involved in the pathogenesis of MS.
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January 2025
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Testing for myelin oligodendrocyte glycoprotein immunoglobulin G antibodies (MOG-IgG) is essential to the diagnosis of MOG antibody-associated disease (MOGAD). Due to its central role in the evaluation of suspected inflammatory demyelinating disease, the last 5 years has been marked by an abundance of research into MOG-IgG testing ranging from appropriate patient selection, to assay performance, to utility of serum titers as well as cerebrospinal fluid (CSF) testing. In this review, we synthesize current knowledge pertaining to the "who, what, where, when, why, and how" of MOG-IgG testing, with the aim of facilitating accurate MOGAD diagnosis in clinical practice.
View Article and Find Full Text PDFViruses
January 2025
Virology Department, Institut Pasteur de Dakar, 36 Avenue Pasteur, Dakar 200, Senegal.
Neurological manifestations associated with human parvovirus B19 (B19V) infections are rare and varied. Acute encephalitis and encephalopathy are the most common, accounting for 38.8% of all neurological manifestations associated with human B19V.
View Article and Find Full Text PDFViruses
January 2025
Programa de Pós-Graduação em Doenças Infecciosas e Parasitárias, Faculdade de Medicina, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-913, Brazil.
Background And Objectives: HTLV-1-associated myelopathy (HAM) is a chronic progressive inflammatory disease of the spinal cord. This study assesses the diagnostic accuracy of the neuroinflammatory biomarkers neopterin and cysteine-X-cysteine motif chemokine ligand 10 (CXCL-10) in cerebrospinal fluid (CSF) for HAM.
Methods: CSF samples from 75 patients with neurological disorders-33 with HAM (Group A), 19 HTLV-1-seronegative with other neuroinflammatory diseases (Group B), and 23 HTLV-1-seronegative with non-neuroinflammatory diseases (Group C)-were retrospectively evaluated.
Viruses
December 2024
Life Sciences, Health, and Engineering Department, The Roux Institute, Northeastern University, Portland, ME 04101, USA.
JC polyomavirus (JCPyV) establishes a persistent, asymptomatic kidney infection in most of the population. However, JCPyV can reactivate in immunocompromised individuals and cause progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease with no approved treatment. Mutations in the hypervariable non-coding control region (NCCR) of the JCPyV genome have been linked to disease outcomes and neuropathogenesis, yet few metanalyses document these associations.
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