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  • Author or Editor: Efthimios Dardiotis x
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Efthimios Dardiotis, Kostas N. Fountas, Maria Dardioti, Georgia Xiromerisiou, Eftychia Kapsalaki, Anastasia Tasiou and Georgios M. Hadjigeorgiou

Traumatic brain injury (TBI) constitutes a major cause of mortality and disability worldwide, especially among young individuals. It is estimated that despite all the recent advances in the management of TBI, approximately half of the patients suffering head injuries still have unfavorable outcomes, which represents a substantial health care, social, and economic burden to societies.

Considerable variability exists in the clinical outcome after TBI, which is only partially explained by known factors. Accumulating evidence has implicated various genetic elements in the pathophysiology of brain trauma. The extent of brain injury after TBI seems to be modulated to some degree by genetic variants.

The authors' current review focuses on the up-to-date state of knowledge regarding genetic association studies in patients sustaining TBI, with particular emphasis on the mechanisms underlying the implication of genes in the pathophysiology of TBI.

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Georgia Xiromerisiou, Efthimios Dardiotis, Vaïa Tsimourtou, Persa Maria Kountra, Konstantinos N. Paterakis, Eftychia Z. Kapsalaki, Kostas N. Fountas and Georgios M. Hadjigeorgiou

Over the past few years, considerable progress has been made in understanding the molecular mechanisms of Parkinson disease (PD). Mutations in certain genes are found to cause monogenic forms of the disorder, with autosomal dominant or autosomal recessive inheritance. These genes include alpha-synuclein, parkin, PINK1, DJ-1, LRRK2, and ATP13A2. The monogenic variants are important tools in identifying cellular pathways that shed light on the pathogenesis of this disease. Certain common genetic variants are also likely to modulate the risk of PD. International collaborative studies and meta-analyses have identified common variants as genetic susceptibility risk/protective factors for sporadic PD.