Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.

NAD+ plays a pivotal role in energy metabolism and adaptation to external stimuli and stressful conditions. A significant reduction in intracellular NAD+ levels is associated with aging and contributes to the development of chronic cardiovascular, neurodegenerative, and metabolic diseases. It is of particular importance to maintain optimal levels of NAD+ in cells with high energy consumption, particularly in the brain.

Neuroanatomical correlates of language impairment in non-fluent variant of primary progressive aphasia.

Introduction: Non-fluent variant of primary progressive aphasia (nfvPPA) is a neurodegenerative disorder with a predominantly speech and language impairment. Apraxia of speech and expressive agrammatisms along with decreased speech fluency and impaired grammar comprehension are the most typical disorder manifestations but with the course of the disease other language disturbances may also arise. Most studies have investigated these symptoms individually, and there is still no consensus on whether they have similar or different neuroanatomical foundations in nfvPPA.

Mitochondrial Dynamics in Brain Cells During Normal and Pathological Aging.

Mitochondrial dynamics significantly play a major role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. The dysregulation of mitochondrial biogenesis and function, characterized by impaired fission and fusion processes mediated by a number of proteins, in particular, Drp1, Mfn1, Mfn2, Opa1, and PGC-1α, contributes to neuronal vulnerability and degeneration. Insufficient mitophagy and disrupted mitochondrial transport exacerbate oxidative stress and neurotoxicity.

High heterogeneity of cross-reactive immunoglobulins in multiple sclerosis presumes combining of B-cell epitopes for diagnostics: a case-control study.

Background: Multiple sclerosis (MS) is a neuroinflammatory disease triggered by a combination of genetic traits and external factors. Autoimmune nature of MS is proven by the identification of pathogenic T cells, but the role of autoantibody-producing B cells is less clear. A comprehensive understanding of the development of neuroinflammation and the identification of targeted autoantigens are crucial for timely diagnosis and appropriate treatment.

Molecular Mechanisms of Spinocerebellar Ataxia Type 17.

Spinocerebellar ataxia type 17 (SCA17) is a hereditary neurodegenerative disorder characterized by progressive motor and cognitive decline, leading to severe disability and death. SCA17 is caused by a CAG repeat expansion mutation in the TBP gene, resulting in the production of an abnormally long polyglutamine tract, which classifies it as a polyglutamine disorder. At present, there is no effective treatment for SCA17, and existing therapies provide only symptomatic relief.