Cerebrolysin concentrate is a medication whose main active ingredient is brain-derived neurotrophic factor. It has been reported to help in the restoration of cognitive function and overall physical function after brain injuries. We present the case of a 72-year-old man with severe oral apraxia due to a left middle cerebral artery ischemic stroke involving the left insular cortex. He was being tube fed due to severe oral apraxia with cognitive decline that made it difficult for him to even imitate simple oral movements. The patient initially had impaired consciousness and cognitive function. He also had limited physical activity due to acute stroke complications, such as hemorrhagic transformation of cerebral infarction, and required bed rest until 23 days after onset. The patient received intravenous cerebrolysin concentrate in addition to intensive rehabilitation therapy from 23 days after onset. After rehabilitation and administration of cerebrolysin concentrate, there was a marked recovery within a short period of time to the point where oral intake of a regular diet was possible, indicating a significant improvement in oral apraxia. It is a notable example of the potential therapeutic effect of cerebrolysin concentrate for post-stroke oral apraxia.

This secondary analysis of the CAPTAIN-RTMS trial data focused on the significance of quantitative electroencephalography (qEEG) indices as indicators of recovery in patients with traumatic brain injury (TBI). By focusing on the delta alpha ratio (DAR), delta theta/alpha beta ratio (DTABR), and theta beta ratio (TBR), this study explored the shifts in brainwave activity as a response to an integrative treatment regimen of repetitive transcranial magnetic stimulation (rTMS) combined with the neurotrophic agent Cerebrolysin. Findings revealed significant increases in DAR and DTABR, suggesting changes in neurophysiological dynamics after treatment. However, variations in TBR were inconclusive in providing clear electrophysiological insights. These results indicate that further research is necessary to describe and understand the underlying mechanisms of brain recovery and to develop refined treatment frameworks for patients with TBI.

What is expected from neuroprotection is to inhibit neuronal death and halt or decelerate the neuronal loss to lower the mortality rates, decrease disability, and improve the quality of life following an acute ischemic stroke. Several agents were described as neuroprotective up to date; however, there is still debate which to use in the neurorehabilitation of stroke patients, in terms of both efficacy and also safety. In this review, we discuss the agents, citicoline, cerebrolysin and MLC901 (NeuroAiD II), the three agents which have started to be used frequently in neurorehabilitation clinics recently in the light of the current literature.

Diabetes mellitus (DM) is a metabolic disorder impacting cerebral function. The administration of Streptozotocin (STZ) is a well-known animal model of insulinopenic type 1 DM in rats. STZ-induced DM results in a myriad of alteration in the periphery and central nervous system (CNS). Cerebrolysin (CBL) is a neuropeptide preparation that promotes synaptic and neuronal plasticity in various animal models. In all cases, CBL was administered when the model was established. This research aims to investigate the neuroprotective and neurorepair effect of CBL on the cytoarchitecture of neurons and spine density in pyramidal neurons of the prefrontal (PFC) and the CA1 region of the dorsal hippocampus, as well as spheroidal neurons of the dentate gyrus (DG), in STZ-induced DM. In the first experimental condition, STZ and CBL are administered at the same time to evaluate the potential preventive effect of CBL. In the second experimental condition, CBL was administered two months after establishing the DM model to measure the potential neurorepair effect of CBL. STZ-induced hyperglycemia remained unaltered by the administration of CBL in both experimental conditions. In the first experimental condition, CBL treatment preserved the neuronal morphology in PFC layer 3, PFC layer 5 and the DG of the hippocampus, while also maintaining spine density in the PFC-3, DG and CA1 hippocampus. Furthermore, CBL induced neurorepair in neurons within the PFC-3, PFC-5 and CA1 regions of the hippocampus, along with an increase in spine density in the PFC-3, DG and CA1 hippocampus. These findings suggest that CBL´s effects on neuroplasticity could be observed before or after the damage was evident.

Post-traumatic stress disorder (PTSD) is a common mental health disorder, with an incidence of up to 12.5% among primary care patients. Most often, PTSD is detected in combat veterans, victims of terrorist attacks and terror, but it can also be a consequence of traumatic brain injury and medical interventions. Impaired cognitive functioning is a key feature of PTSD, including attention deficits and reduced processing speed, executive dysfunction, and impairments in verbal learning and memory. Cognitive impairments in PTSD are significantly persistent and are largely similar in nature to neuropsychological impairments in neurodegenerative pathology. Possible pathogenetic mechanisms underlying PTSD are the development of neuroinflammation, oxidative stress and decreased production of neurotrophic factors. One of the promising areas of treatment is the use of Cerebrolysin, which has powerful neurotrophic and anti-inflammatory activity.
Посттравматическое стрессовое расстройство (ПТСР) является распространенной психической патологией, частота которой среди пациентов первичной медико-санитарной помощи достигает 12,5%. Наиболее часто ПТСР выявляется у ветеранов боевых действий, жертв терактов, однако также может быть следствием черепно-мозговой травмы, медицинских вмешательств. Нарушение когнитивных функций является ключевой особенностью ПТСР, включающей дефицит внимания и снижение скорости обработки информации, исполнительную дисфункцию, а также нарушение вербального обучения и памяти. Когнитивные нарушения при ПТСР отличаются значительной стойкостью и по своему характеру во многом схожи с нейропсихологическими нарушениями при нейродегенеративной патологии. Возможными патогенетическими механизмами, лежащими в основе ПТСР, являются развитие нейровоспаления, оксидантный стресс и снижение выработки нейротрофических факторов. Одно из перспективных направлений лечения — применение Церебролизина, обладающего мощной нейротрофической и противовоспалительной активностью.

Neurological disorders, ranging from acute forms such as stroke and traumatic brain injury to neurodegenerative diseases like dementia, are the leading cause of disability-adjusted life years (DALYs) worldwide. A promising approach to address these conditions and promote nervous system regeneration is the use of the neuropeptide preparation Cerebrolysin, which has been shown to be effective in both clinical and preclinical studies. Despite claims of similar clinical efficacy and safety by several peptide preparations, concerns regarding their generic composition and efficacy have been previously raised. Based on these reports, we analyzed the peptide composition and neurotrophic activity of several peptide preparations allegedly similar to Cerebrolysin and approved in some countries for treating neurological diseases. Our results demonstrate that these preparations lack relevant biological activity and that the peptide composition is significantly different from Cerebrolysin. peptide.

Stroke is one of the leading causes of disability worldwide, where the Hippocampus (HPC) is affected. HPC organizes memory, which is a cognitive domain compromised after a stroke, where cerebrolysin (CBL) and Nicotinamide (NAM) have been recognized as potentially therapeutic. In this study, we aimed to evaluate the efficacy of a combined administration of CBL and NAM in a rat stroke model. Male Sprague-Dawley rats (n = 36) were divided into four groups: saline (pMCAO - Saline), CBL (pMCAO + CBL), NAM (pMCAO + NAM), and experimental (pMCAO + CBL-NAM) (n = 9 per group). A permanent middle cerebral artery occlusion (pMCAO) was induced through electrocauterization of the middle cerebral artery, followed by the administration of CBL (2.5 ml/kg), NAM (500 mg/kg) or combined immediately after skin suture, as well as at 24, 48, and 72 h post-surgery. The rats were evaluated in the novel object recognition test; hippocampal infarct area measurement; reconstruction of neurons from CA1 for Sholl analysis; and, measurement of brain-derived neurotrophic factor (BDNF) levels near the infarct zone. Our findings revealed that the administration of CBL or NAM induced infarct reduction, improved cognition, and increased BDNF levels. Moreover, a combination of CBL and NAM increased dendritic intersection in CA1 pyramidal neurons. Thus, the combined administration of CBL and NAM can promote cognitive recovery after a stroke, with infarct reduction, cytoarchitectural changes in HPC CA1 neurons, and BDNF increase. Our findings suggest that this combination therapy could be a promising intervention strategy for stroke.

OBJECTIVE: The aim of this study is to evaluate radioprotective effects of Cerebrolysin (CBL) in rats\' brain tissues after local irradiation.
BACKGROUND: CBL has demonstrated antioxidant, anti-inflammatory, and tissue repair properties. In this study, the radioprotective effects of CBL in the brain tissues of rats after Irradiation (IR) (50 mg/ kg) were evaluated.
OBJECTIVE: The levels of different oxidative stress markers, including malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) were examined after treatment with radiation and CBL.
METHODS: First, 20 male adult Wistar rats weighing 180-200 g were used. The animals were exposed to a single fraction of 15Gy using a linear accelerator unit at a dose rate of 200 cGy/mine. In this study, to check the amount of oxidative stress following the IR, the level of four markers MDA, NO, GPx, CAT, and SOD were examined and measured using the spectrophotometric method and purchased kits.
RESULTS: The results showed that compared to the IR group, the administration of CBL increases the levels of GPX and SOD significantly (p < 0.05).
CONCLUSIONS: Our finding suggests that CBL has radioprotective effects on the brain by enhancing antioxidant defense mechanisms.

Numerous clinical trials involving natural products have been conducted to observe cognitive performances and biomarkers in Alzheimer\'s Disease (AD) patients. However, to date, no natural-based drugs have been approved by the FDA as treatments for AD. In this review, natural product-based compounds that were tested in clinical trials from 2011 to 2023, registered at www.clinicaltrials.gov were reviewed. Thirteen compounds, encompassing 7 different mechanisms of action were covered. Several observations were deduced, which are: i) several compounds showed cognitive improvement, but these improvements may not extend to AD, ii) compounds that are endogenous to the human body showed better outcomes, and iii) Docosahexaenoic acid (DHA) and cerebrolysin had the most potential as AD drugs among the 13 compounds. Based on the current findings, natural products may be more suitable as a supplement than AD drugs in most cases. However, the studies covered here were conducted in a relatively short amount of time, where compounds acting on AD pathways may take time to show any effect. Given the diverse pathways that these natural products are involved in, they may potentially produce synergistic effects that would be beneficial in treating AD. Additionally, natural products benefit from both physicochemical properties being in more favorable ranges and active transport playing a more significant role than it does for synthetic compounds.

Amyotrophic lateral sclerosis (ALS) is a devastating and progressive neurodegenerative disease with limited treatment options available. Cerebrolysin is a drug candidate for the treatment of ALS because of its neuroprotective and neuroregenerative effects. We initiated a pilot clinical study of a combination of Cerebrolysin and riluzole to assess the therapeutic benefit of Cerebrolysin as an add-on treatment on clinical signs and symptoms in outpatients with ALS. Twenty patients with a clinically definitive diagnosis of ALS were enrolled and randomly assigned in a 1:1 ratio to receive Cerebrolysin or placebo. All patients received 50 mg of riluzole PO twice daily as a standard treatment. Patients in the Cerebrolysin group received intravenous injections of 10 mL of Cerebrolysin once daily, five days a week for the first month and three days a week for the next two months. Analysis of the ALS Functional Rating Scale - revised at Month 1 (primary outcome measure), showed a significant treatment effect in favor of Cerebrolysin with a 2.3-point improvement from baseline to Month 1 compared to a 0.9-point decrease in patients on placebo (P=0.005). The effect was maintained over the three-month study period, and the beneficial effect of Cerebrolysin over placebo was also evident in the secondary outcome measures. The safety analysis showed that the combination of riluzole and Cerebrolyisn was well tolerated. Our results demonstrate for the first time a significant clinical effect of Cerebrolysin in improving functional outcomes in patients with ALS and suggest that Cerebrolysin has potential as a novel therapeutic option for ALS.