Intracerebral Hemorrhage: Advances in Preclinical Studies: 2nd Edition
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".
Deadline for manuscript submissions: 31 August 2025 | Viewed by 2137
Special Issue Editor
Interests: intracerebral hemorrhage; cerebral edema; neuroinflammation; oxidative stress; neurodegeneration; excitotoxicity; blood components; neurotoxicity; neurological deficits; blood–brain barrier damage; infiltrating macrophages; glial activation
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Special Issue Information
Dear Colleagues,
Intracerebral hemorrhage (ICH) is a major public health problem and severe subtype of stroke characterized by cerebral bleeding. In comparison to other stroke subtypes, ICH is associated with the highest mortality and morbidity rates. Additionally, the incidence of ICH is expected to increase due to aging and the increasing use of anticoagulants. To date, there is no effective treatment for ICH, making it the deadliest subtype of stroke.
ICH results in severe brain injury, which is categorized into primary and secondary brain damage. The primary brain damage is mainly attributed to the mass effect of the hematoma, whereas the mechanisms of the secondary brain damage include, but are not limited to, neuroinflammation, oxidative stress, apoptosis, and excitotoxicity. The secondary brain injury, which persists for a longer period, contributes to long-term neurological deficits and is considered a viable target for therapeutic intervention. However, given the complex pathophysiology of ICH, further elucidation of the brain injury mechanisms is imperative for the identification of novel molecular targets for therapeutic intervention.
Herein, we attempt to provide an update on ICH by inviting reviews, research articles, and short communications for the Special Issue entitled “Intracerebral Hemorrhage: Advances in Preclinical Studies”.
We look forward to your contributions.
Dr. Sangeetha Sukumari-Ramesh
Guest Editor
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Keywords
- neuroinflammation
- oxidative stress
- neurodegeneration
- neurological deficits
- blood–brain barrier damage
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