Brain Ischemia: From Molecular Mechanisms to Innovative Therapies
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 30 December 2025 | Viewed by 116
Special Issue Editor
Interests: brain ischemia; Alzheimer's disease; brain ischemia versus Alzheimer’s disease; amyloid precursor protein; amyloid; tau protein; secretases; presenilins; synuclein; apolipoproteins A1; E and J; autophagy; mitophagy; apoptosis; LRP1; RAGE; neuroinflammation; genes; neurodegeneration; dementia
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Special Issue Information
Dear Colleagues,
Focal or global brain ischemia leads to neuronal death and brain atrophy, which in turn results in the genomic and proteomic changes characteristic of Alzheimer's disease, including amyloid and tau protein alterations. Identical injuries are triggered by perinatal hypoxia, which intensifies changes in the brain later in life, leading to impaired cognitive functions and dementia. There is also current data indicating an association with amyloid or tau protein in pathological changes in the brain following traumatic brain injury and apnea leading to severe neurodegenerative changes with impaired cognitive functions and the development of dementia. Currently, there is increasing evidence that the pathologies caused by the above diseases, especially with the extension of the age of observation, are almost identical to the neurodegenerative changes occurring in Alzheimer's disease. The above disorders and Alzheimer's disease share common pathological features, such as amyloid plaques and neurofibrillary tangles, neuronal loss, neuroinflammation, brain atrophy, and dementia. The neuropathology of these diseases and whether they precede the development of Alzheimer's disease is the subject of ongoing research. In this Special Issue, I would like to learn more about each common proteomic and genomic pathway and mechanism of the above diseases as they relate to Alzheimer's disease. I would like to focus on the mechanisms that initiate neurodegeneration at the level of genomic, proteomic, and secondary cascades. The start of the genome-wide era and the recent progress made in the genetics field have given an approach to find biomarkers and potential drug targets related to the above disorders. Genome-wide association studies are powerful tools to identify genetic variants associated with a trait of interest. These studies allow rapidly scanning markers across the genome of larger population samples, interrogating more than hundreds of thousands of genetic variations across the genome. I hope that new mechanisms/hypotheses regarding the development of neurodegeneration in Alzheimer's disease will be presented and discussed in the context of the above conditions as risk factors or etiology. In this issue, I invite scientists and physicians involved in the study of brain injuries to participate in an update of clinical and experimental research aimed at finding new therapeutic options for neuron regeneration after brain injuries. I hope that each article on this topic will both inform and stimulate interest in the mechanisms that explain the development of dementia following asphyxia, traumatic brain injury, and especially brain ischemia and Alzheimer's disease.
Prof. Dr. Ryszard Pluta
Guest Editor
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Keywords
- ischemic neurodegeneration
- focal brain ischemia
- global brain ischemia
- perinatal asphyxia
- ischemic stroke
- traumatic brain injury
- apnea
- neuroinflammation
- proteins
- genes
- genes involved in neurodegeneration
- glia-to-neurons genetic conversion
- dementia
- Alzheimer’s disease
- genetic conversion of ischemia to Alzheimer's disease
- new therapeutic approaches
- biomarkers
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