Accumulating data shows that oxidative stress plays a crucial role in neurodegenerative disorders. The literature data indicate thatin vivoor postmortem cerebrospinal fluid and brain tissue levels of F₂-isoprostanes (F₂-IsoPs) especially F₄-neuroprotanes (F₄-NPs) are significantly increased in some neurodegenerative diseases: multiple sclerosis, Alzheimer's disease, Huntington's disease, and Creutzfeldt-Jakob disease. Central nervous system is the most metabolically active organ of the body characterized by high requirement for oxygen and relatively low antioxidative activity, what makes neurons and glia highly susceptible to destruction by reactive oxygen/nitrogen species and neurodegeneration. The discovery of F₂-IsoPs and F₄-NPs as markers of lipid peroxidation caused by the free radicals has opened up new areas of investigation regarding the role of oxidative stress in the pathogenesis of human neurodegenerative diseases. This review focuses on the relationship between F₂-IsoPs and F₄-NPs as biomarkers of oxidative stress and neurodegenerative diseases. We summarize the knowledge of these novel biomarkers of oxidative stress and the advantages of monitoring their formation to better define the involvement of oxidative stress in neurological diseases.

Nutrition and rehabilitation are crucial in post-stroke recovery, especially in the elderly. Since stroke is the leading cause of long-term disability, there is a need to promote special, individually tailored nutrition strategies targeting older patients with low motor ability. Chronic stroke survivors have higher risk of developing nutrition-related chronic diseases, such as sarcopenia, anemia, type 2 diabetes mellitus and osteoporosis. Moreover, reduced motor activity, cognitive impairment and depression might be aggravated by poor malnutrition status. Accumulated data suggest that nutritional supplements and neuroprotective diets can be associated with better effectiveness of post-stroke rehabilitation as well as brain recovery. Therefore, this review focuses on preventive strategies that can improve dietary intake and change dietary patterns. We highlight the importance of neuroprotective diets, the problem of dysphagia and the role of nutrition in rehabilitation. This article focuses on potential nutritional supplements and neuroprotective diets that may have an impact on functional recovery during and after rehabilitation. Moreover, a new approach to post-stroke neuroplasticity including the use of agents from marine sources such as fucoxanthin and tramiprosate as compounds that might be used as potential neuroprotectants with antioxidative and anti-inflammatory properties is introduced.

Neuroplasticity is a natural process occurring in the brain for the entire life. Stroke is the leading cause of long term disability and a huge medical and financial problem throughout the world. Research conducted over the past decade focused mainly on neuroprotection in the acute phase of stroke while very little studies target the chronic stage. Recovery after stroke depends on the ability of our brain to reestablish the structural and functional organization of neurovascular networks. Combining adjuvant therapies and drugs may enhance the repair processes and restore impaired brain functions. Currently, there are some drugs and rehabilitative strategies that can facilitate brain repair and improve clinical effect even years after stroke onset. Moreover, some of the compounds such as citicoline, fluoxetine, niacin, levodopa, etc. are already in clinical use or are being trialed in clinical issues. Many studies are also testing cell therapies; in our review, we focused on studies where cells have been implemented at the early stage of stroke. Next, we discuss pharmaceutical interventions. In this section, we selected methods of cognitive, behavioral, and physical rehabilitation as well as adjuvant interventions for neuroprotection including noninvasive brain stimulation and extremely low-frequency electromagnetic field. The modern rehabilitation represents a new model of physical interventions with the limited therapeutic window up to six months after stroke. However, previous studies suggest that the time window for stroke recovery is much longer than previously thought. This review attempts to present the progress in neuroprotective strategies, both pharmacological and non-pharmacological that can stimulate the endogenous neuroplasticity in post-stroke patients.

Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS). The etiology of this multifactorial disease has not been clearly defined. Conventional medical treatment of MS has progressed, but is still based on symptomatic treatment. One of the key factors in the pathogenesis of MS is oxidative stress, enhancing inflammation and neurodegeneration. In MS, both reactive oxygen and nitrogen species are formed in the CNS mainly by activated macrophages and microglia structures, which can lead to demyelination and axon disruption. The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10). The early stage of MS (RRMS) lasts about 10 years, and is dominated by inflammatory processes, whereas the chronic stage is associated with neurodegenerative axon and neuron loss. Since oxidative damage has been known to be involved in inflammatory and autoimmune-mediated processes, antioxidant therapy could contribute to the reduction or even prevention of the progression of MS. Further research is needed in order to establish new aims for novel treatment and provide possible benefits to MS patients. The present review examines the roles of oxidative stress and non-pharmacological anti-oxidative therapies in MS.

Multiple sclerosis (MS) is a chronic, immune-mediated disease and the leading cause of disability among young adults. MicroRNAs (miRNAs) are involved in the post-transcriptional regulation of gene expression. Of them, miR-155 is a crucial regulator of inflammation and plays a role in modulating the autoimmune response in MS. miR-155 is involved in blood–brain barrier (BBB) disruption via down-regulation of key junctional proteins under inflammatory conditions. It drives demyelination processes by contributing to, e.g., microglial activation, polarization of astrocytes, and down-regulation of CD47 protein and affecting crucial transcription factors. miR-155 has a huge impact on the development of neuropathic pain and indirectly influences a regulatory T (Treg) cell differentiation involved in the alleviation of pain hypersensitivity. This review also focused on neuropsychiatric symptoms appearing as a result of disease-associated stressors, brain atrophy, and pro-inflammatory factors. Recent studies revealed the role of miR-155 in regulating anxiety, stress, inflammation in the hippocampus, and treatment-resistant depression. Inhibition of miR-155 expression was demonstrated to be effective in preventing processes involved in the pathophysiology of MS. This review aimed to support the better understanding the great role of miR-155 dysregulation in various aspects of MS pathophysiology and highlight future perspectives for this molecule.

Neurodegeneration is the hallmark of many chronic progressive neurogical disorders characterized by specific clinical, morphological and biochemical features. Central nervous system is very sensitive to oxidative stress, which is considered as a key factor of neurodegenerative disorders. Therefore, many therapeutical strategies are focused on molecules with redox activity to re-establish the equilibrium between pro and antioxidants. Due to the fact that melatonin readily crosses the blood- brain-barrier, concomitant with its safety profile at the highest dosages makes this dietary supplement very useful in possible clinical application in neurodegeneration. Melatonin is currently marketed in several countries as a dietary supplement with no prescription. Clinical trials have shown different effectiveness of melatonin supplementation in several disorders, including neurodegenerative disorders. Melatonin has unique biochemical properties such as scavenging of hydroxyl, carbonate, alkoxyl, peroxyl and aryl cation radicals and stimulation of activities main antioxidative enzymes (glutathione peroxidase, superoxide dismutase etc.). Moreover, it can suppress nitric oxide synthase. The present paper highlighted the potential clinical role of melatonin in main neurodegenerative diseases including Alzheimer disease, Parkinson disease, amylotrophic lateral sclerosis and multiple sclerosis. Moreover, in this review the main molecular aspects of melatonin in brain cell protection and survival mechanisms were discussed. Therefore, melatonin is regarded as a potential therapeutical agent in clinical application in neurodegenerative disorders, but this findings needs to be confirmed by the larger, more well-designed clinical trials.