Traumatic Brain Injury/Chronic Traumatic Encephalopathy as Cause of Alzheimer’s Disease: Physics and Molecular Biology in the Genesis of Neurodegeneration?
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: 20 September 2024 | Viewed by 1579
Special Issue Editor
Interests: neurooncology; neurodegenerative diseases; traumatic brain injury/chronic traumatic encephalopathy; demyelinating diseases; neurodevelopmental disorders; neuromuscular disorders
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Special Issue Information
Dear Colleagues,
Background
Neurodegenerative diseases encompass a group of nosological entities that manifest either as a decline in the cognitive capacity (e.g. Alzheimer’s Disease [AD], Fronto-Temporal Dementia [FTD], Lewy Body Dementia [LBD]) or as an altered motor function with variable but disordered movement patterns (e.g. Parkinson’s Disease [PD], Huntington’s Disease [HD], Multiple System Atrophy [MSA]) of the affected individuals. The etiological factor behind all these well recognised clinical presentations is the substantial degeneration of the neurons, whether these are located within the brain or the spinal cord. Several intra- (e.g. neurofibrillary tangles [NFTs], Lewy bodies) and extracellular deposits (e.g. senile [neuritic] plaques) have been described until now and they have been implicated in the damage of the neuronal cells. Furthermore, specific protein aggregates have been found as components of these abnormal structures. Thus, it has been revealed that neurofibrillary tangles contain hyperphosphorylated tau-protein, Lewy bodies comprise a-synuclein, while senile [neuritic] plaques are composed mainly by b-amyloid accumulates. Recently, scientific society has paid particular attention to conditions named traumatic brain injury (TBI) and chronic traumatic encephalopathy (CTE; the neurobehavioral profile after the occurrence of repeated TBIs), as these has been shown to be associated with some of the above described neurodegenerative diseases (e.g. Alzheimer’s disease, Parkinson’s disease). In particular, common features described both in TBI/CTE and Alzheimer’s disease include dementia as well as morphological changes, both at the macroscopic level with brain atrophy and at the microscopic level with the presence of phosphorylated tau inclusions and senile [neuritic] plaques.
Summary
Although a lot of progress has been attained during the last few years in the field of neurodegenerative diseases, the actual pathogenetic mechanism that leads to their development has not been fully elucidated. In this context, several studies have also tried to understand whether there is a connection between Traumatic Brain Injury (TBI)/Chronic Traumatic Encephalopathy (CTE) and Alzheimer’s disease, considering their similarities in the clinical manifestations and histopathological characteristics, but without the expected outcome. Thus, the question that has to be answered still remains; could physical stress, in the form of a brain trauma (TBI/CTE), be the reason for the subsequent biological changes taking place inside the neurons, leading substantially to their damage and death (manifested as Alzheimer’s disease)? In other words, is it possible to establish a "cause-effect" relationship, between TBI/CTE (cause) and Alzheimer’s disease (effect)? “Hic Rhodus, hic salta”.
Prof. Dr. Dimitrios Kanakis
Guest Editor
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Keywords
- traumatic brain injury (TBI)
- chronic traumatic encephalopathy (CTE)
- head impacts
- Alzheimer's disease (AD）
- neurodegeneration
