About this Research Topic
Together with the increase in life expectancy, the prevalence of age-related disorders, including neurodegenerative diseases, is growing. In spite of the scale of the problem, the etiology of most neurodegenerative disorders remains unclear, and as a consequence, there are no effective treatments stopping or at least slowing down their progression. There is growing evidence that pathophysiology of different neurodegenerative diseases may overlap at multiple molecular levels and pathways ultimately leading to cell death.
Understanding the neural networks and their involvement in neurodegenerative conditions could provide better insights into the principles of neurodegeneration.
It is well known, that many contributing factors i.e. inflammatory processes, oxidative damage, mitochondrial impairment, pathogenic proteins, apoptosis and autophagy dysfunction – all well-established features of neurodegeneration – are not exclusively related to any particular neurodegenerative disorder and identified in both sporadic and familial forms.
Oxidative stress and inflammation, which are tightly linked and interdependent, are regarded as playing a key role in neurodegeneration pathogenesis. This is why maintaining the redox balance, based on the generation and elimination of reactive oxygen species by endogenous and exogenous sources is crucial for neuroprotection. Recently, it has become widely accepted that chronic activation of the immune response, particularly mediated by microglia, can evoke neurotoxic pathways finally leading to neurodegeneration. However again, on the other hand, the immune system plays a crucial role in maintaining neuroprotection and regenerative processes. Last but not least, a growing number of studies point out the importance of intestinal inflammation as a potential culprit in neurodegenerative conditions.
In most neurodegenerative diseases, there is also overwhelming evidence of impaired mitochondrial function as a causative factor. It is not surprising, as the overproduction of reactive oxygen species can contribute to the damage of mitochondrial respiratory chain, membrane permeability, and interfere with the calcium homeostasis.
Another common feature of neurodegeneration is the accumulation of various pathogenic proteins in neural cells, being postulated to spread via similar mechanisms and finally contributing to cell death.
Finally, the balance between cell death and survival evoked by inflammatory processes depends on the checkpoint committing the cells either to the pro-survival autophagy as the self-defense mechanism, either to inevitable death mediated by apoptosis.
Identifying particular proteins and pathways as convergence points in the development of neurodegenerative diseases seems to be fundamental to the understanding of their causes and mechanisms and may help to define new targets for neuroprotective therapies.
Therefore, in this Research Topic, we would like to gather articles summarizing current in-vitro or in vivo investigations not particularly focusing on specific disease and the neural populations directly responsible for symptomatology, but rather more general, linking i.e. the immune system and oxidative stress in brain aging and neurodegeneration, glial responses and neuroinflammation in neurodegenerative diseases, innate immune system, and neurodegeneration.
We particularly encourage the submission of studies related to putative etiological models of neurodegenerative processes, not restricted to identified causative mutations but based upon mentioned above assumptions and current trials in the development of the use of antioxidants in neuroprotective strategies together with modulating the immune system.
Keywords: Neurodegeneration, inflammation, oxidative stress, gut-brain axis, neuroprotection, glial response, innate immune system
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