Cerebroprotein Hydrolysate

Stroke is a pathology related to the vascular system in the brain and it is one of the main causes of disability, representing a burden on public health. This lesion provokes a disorganization of sensory-motor and cognitive systems, the latter associated with hippocampal activity, a structure in which α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and NMDA N-methyl-D-aspartate (NMDA) receptors are important for the integration of information. Several molecules have been studied for their capacity to enhance recovery from a stroke, including cerebrolysin that could potentially be reinforced by environmental enrichment. Here, stroke was induced in 40 male rats and 24 h later, they were administered cerebrolysin (2.5 ml/kg), put in an environmentally enriched arena or given both treatments, for 10 days. Subsequently, motor functioning was assessed with the Bederson test and the cognitive domain was assessed through novel object recognition. Hematoxylin/eosin staining was then used to assess the infarct size, and AMPA-GRIA1 and NMDA-R1 subunits in the hippocampus were measured by ELISA. In motor and cognitive performance, the administration of cerebrolysin and environmental enrichment enhanced recovery. Moreover, the infarct size decreased in all the groups that received a treatment, but an increase occurred in AMPA-GRIA1 only in experimental group regarding to control group, while NMDA-R1 had no differences. These results suggest that cerebrolysin and environmental enrichment could act in synergy to recover after a stroke, leading to a smaller infarct area and the presence of more AMPA-GRIA1 subunits in the hippocampus of experimental group. These data encourage further studies in which neurorehabilitation approaches can be combined with cerebrolysin administration to treat the motor and cognitive symptoms of stroke.

The article examines the potential role of brain mechanical damage as a trigger for the development of neurodegenerative changes. Attention is paid to dysfunction of the neurovascular unit, and disruption of the functional and compensatory capabilities of blood flow. The importance of microhemorrhages that occur in the acute period of injury and the formation of first focal and then diffuse neuroinflammation is emphasized. The importance of mitochondrial dysfunction was separately determined as a significant factor in increasing the risk of developing Alzheimer's disease (AD) in patients after traumatic brain injury (TBI). In TBI, there is a decrease in the expression of tight junction (TC) proteins of endothelial cells, such as occludin, claudin, JP, which leads to increased permeability of the blood-brain barrier. TBI, provoking endothelial dysfunction, contributes to the development of metabolic disorders of β-amyloid and tau protein, which in turn leads to worsening vascular damage, resulting in a vicious circle that can ultimately lead to the development of AD and dementia. Age-related changes in cerebral arteries, which impair perivascular transport of interstitial fluid, are currently considered as an important part of the «amyloid cascade», especially against the background of genetically mediated disorders of glial membranes associated with defective aquaporin-4 (encoded by the APOE4). Studies in animal models of TBI have revealed an increase in tau protein immunoreactivity and its phosphorylation, which correlates with the severity of injury. A comprehensive analysis of research results shows that the cascade of reactions triggered by TBI includes all the main elements of the pathogenesis of AD: disorders of energy metabolism, microcirculation and clearance of cerebral metabolic products. This leads to a disruption in the metabolism of amyloid protein and its accumulation in brain tissue with the subsequent development of tauopathy. Cerebrolysin, by modulating the permeability of the blood-brain barrier, blocks the development of neuroinflammation, reduces the accumulation of pathological forms of proteins and may be slow down the progression of neurodegeneration.