About the Journal

Brain Pathology is a peer-reviewed bi-monthly, Open Access journal that includes original research, review articles and symposia focusing on the pathogenesis of neurological disease.

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  • Enjoy an easy, Free Format submission process with no color charges, and manuscript transfer option.
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  • Increased impact via Mini Symposium and Virtual Issue publication.

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Articles

RESEARCH ARTICLE
Open access

Ranking and filtering of neuropathology features in the machine learning evaluation of dementia studies

  •  19 February 2024

Graphical Abstract

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Methodology for dementia classification using CFAS and ADNI datasets. The dementia classification methodology was developed and executed in three key stages: design, implementation, and evaluation. After acquiring neuropathology data, we carried out pre-processing and determined the correlation between different features. Utilising seven filter methods, we ranked all neuropathological features. Subsequently, we explored the connection between feature–feature correlation and feature ranking across all applied filter methods. Thereafter, classifiers were evaluated using various feature subsets, depending on their interrelations.

RESEARCH ARTICLE
Open access

Astrocyte‐derived Interleukin‐31 causes poor prognosis in elderly patients with intracerebral hemorrhage

  •  14 February 2024

Graphical Abstract

Description unavailable

High concentrations of astrocyte-derived IL31 in the central nervous system (CNS) immune microenvironment of elderly intracerebral hemorrhage (ICH) patients lead to neurological deficits and poor prognosis. The massive activation of astrocytes after ICH in aged mice releases IL31, which binds to microglia indicating that IL31R binds to each other causing massive chemotaxis of microglia. Subsequent activation of N-methyl-D-aspartic acid receptor (NMDA) receptors, P65 and P53, and so forth, causes degenerative changes in neurons, resulting in neuronal apoptosis and leading to a malignant outcome. In contrast, young mice are more inhibited NMDA receptor, P65 and P53, and so forth, which reduce neuronal apoptosis and thus promotes the recovery of neurological function.

RESEARCH ARTICLE
Open access

Transient receptor potential vanilloid 1 inhibition reduces brain damage by suppressing neuronal apoptosis after intracerebral hemorrhage

  •  2 February 2024

Graphical Abstract

Description unavailable

Inhibition of transient receptor potential vanilloid 1 (TRPV1) significantly reduced brain tissue damage and cerebral inflammation and limited neurodegeneration after ICH. Inhibition of TRPV1 attenuated hemin-induced apoptosis and preserved mitochondrial integrity by reducing Ca2+ influx and CaMKII-P38 and c-Jun NH2-terminal kinase mitogen-activated protein kinase signaling in vitro. Inhibition of TRPV1 may protect against ICH-induced brain injury by modulating mitochondria-related neuronal apoptosis and inflammatory responses.

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