Treatment Of Memory Disorders Research Articles

Potential role of oxytocin in the regulation of memories and treatment of memory disorders

Oxytocin (OXT) is an “affiliative” hormone or neurohormone or neuropeptide consists of nine amino acids, synthesized in magnocellular neurons of paraventricular (PVN) and supraoptic nuclei (SON) of hypothalamus. OXT receptors are widely distributed in various region of brain and OXT has been shown to regulate various social and nonsocial behavior. Hippocampus is the main region which regulates the learning and memory. Hippocampus particularly regulates the acquisition of new memories and retention of acquired memories. OXT has been shown to regulate the synaptic plasticity, neurogenesis, and consolidation of memories. Further, findings from both preclinical and clinical studies have suggested that the OXT treatment improves performance in memory related task. Various trials have suggested the positive impact of intranasal OXT in the dementia patients. However, these studies are limited in number. In the present study authors have highlighted the role of OXT in the formation and retrieval of memories. Further, the study demonstrated the outcome of OXT treatment in various memory and related disorders.

A REVIEW ON THE MEMORY POTENTIAL EFFECT OF “POLYGALA TENUIFOLIA, LYCII FRUCTUS AND CENTELLA ASIATICA”

Traditional medicines have been used as memory enhancers worldwide since ancient times. There are a number of herbs used for this purpose due to their memory potential property. Sage, Ginkgo Biloba, brahmi, ginseng, cinnamon, ginger, rosemary, Salvia Herbs, and Chinese celery are some examples of memory enhancer plants. In this article, we have reviewed the role of three medicinal plants (Polygala tenuifolia, Lycii fructus, and Centella asiatica) in the treatment of memory disorders. These plants have magical effects to increase memory function. There are several studies that show their memory potential effect.

Dihydroxytrimethoxyflavone possess memory improvement effects against scopolamine in mice via modulating multiple pathways: In‐silico and in‐vivo evidences

AbstractBackgroundDementia is a deliberating neurodegenerative disorder which causes impairment of intellectual functions. The USFDA approved drugs has limited efficacy and numerous side effects. Thus, finding newer drugs to manage dementia and cognitive disorders is certainly required. The present study explores the potential of a natural flavone, 5,7‐dihydroxy‐3',4',5'‐trimethoxyflavone (DHF), as memory enhancer drug against scopolamine‐induced cognitive deficit in mice.MethodsAnimals were treated with DHF (5‐10 mg/kg, p.o.) for 7 days after inducing cognitive impairment by scopolamine (1mg/kg,i.p.). Memory functions (passive shock avoidance task and Morris Water Maze), brain acetylcholinesterase (AChE) activity, inflammatory markers, oxidative stress, apoptotic biomarkers and histopathological studies (H&E and congo red staining for beta amyloid) were determined to measure memory improvement effects of DHF. In‐silico (molecular docking) studies were performed to understand the interactions of DHF with key pathological enzymes related to dementia.ResultsTreatment of scopolamine administered mice with DHF improved scopolamine‐induced cognitive impairment and restore brain biochemical parameters (inhibited acetylcholinesterase activity, enhanced glutathione levels, and reduced TBARS, TNF‐α, IL‐6, IL‐1β and caspase‐3 levels). Moreover, histopathological studies showed that DHF treatment reduced the neuronal cell death and amyloid depositions in mice brain. Further, molecular docking studies revealed string interactions of DHF with crucial amino acids of AChE and caspase‐3.ConclusionThese results suggest that DHF was effective in treating scopolamine induced cognitive deficit by improving cerebral cholinergic dysfunction and reducing brain oxidative stress, inflammation, apoptosis and beta‐amyloid depositions in mice. Thus, DHF could be developed as a potential alternative drug to treat memory disorders.

Memory and Traumatic Brain Injury: Assessment and Management Practices of Speech-Language Pathologists.

Memory impairments are among the most commonly reported deficits and among the most frequent rehabilitation targets for individuals with traumatic brain injury (TBI). Memory and learning are also critical for rehabilitation success and broader long-term outcomes. Speech-language pathologists (SLPs) play a central role in memory management for individuals with TBI across the continuum of care. Yet, little is known about the current practice patterns of SLPs for post-TBI memory disorders. This study aims to examine the clinical management of memory disorders in adults with TBI by SLPs and identify opportunities to improve post-TBI memory outcomes. SLPs from across the continuum of care were recruited to complete an online survey. The survey assessed key practice areas specific to memory and memory disorders post-TBI, including education and training, knowledge and confidence, and assessment and treatment patterns. Surveys from 155 SLPs were analyzed. Results revealed that TBI-specific training remains low in the field. Respondents varied in their practice patterns in assessing and treating memory disorders. Most SLPs do not appear to have access to appropriate standardized assessments to measure unique forms of memory. Respondents also reported a range of barriers and opportunities to advance memory outcomes following TBI and provided suggestions of areas in which they would like to see more basic and clinical research. These findings establish a baseline of the current practices for clinical management of memory impairment in adults with TBI by SLPs. Improved opportunities for clinician training, the development of a single tool to assess multiple forms of memory, better access to existing memory assessments, and implementation of evidence-based interventions promise to lead to improved memory outcomes for individuals with TBI.

A Game-based Psychotherapy Intervention Model for Memory Disorder: Model Validation Using EEG Neurofeedback Data

Game-based psychotherapy intervention is a promising alternative to non-pharmacological approaches in treating memory disorders. Nevertheless, the game-based approach is yet to be included systematically in existing intervention models for treating memory disorders. Hence, this article discusses how a proposed gamebased psychotherapy intervention is developed and validated using neurofeedback approach. The proposed model consists of nine exogenous and six instantaneous factors as the main components. To ensure its applicability, a validation procedure has been carried out through a series of psychotherapy experiments involving the elderly with memory disorder symptoms. Electroencephalogram (EEG) data captured from the experiments are thoroughly analysed to validate relationships among factors in the model. Experimental findings have proven that all relationships are successfully validated and supported except for the belief component with the cut-off point of 56.6%. The novelty of this study can be attributed to the integration of digital games and neurofeedback in psychotherapy for memory disorders. The model is believed to be a guideline in planning suitable cognitive training and rehabilitation for people with memory disorders towards improving the quality of the elderly life.

Neuropharmacological studies of ethanolic extract of Vaccinium corymbosum on Alzheimer’s type dementia and catatonia in Swiss albino mice

Introduction: Neuroactive herbal drugs enriched with antioxidants are valuable in treating neurocognitive dysfunction and Vaccinium corymbosum, enriched with antioxidant phytochemicals, is used for treating memory disorders. Hence, the present study evaluated the neuroprotective effects of ethanolic extract of Vaccinium corymbosum (EEVC) on aluminium chloride(AlCl3)-induced Alzheimer’s type of dementia and haloperidol-induced catalepsy-associated behavioural changes. Methods:In vitro antioxidant potential was evaluated using 1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid) (ABTS). The total phenolic content (TPC) was quantified. For in vivo studies, AlCl3 (100 mg/kg) was orally administered for 42 days, whereas the EEVC was administered on the 21st day until the 42nd day in two doses (200 mg/kg and 400 mg/kg). In the haloperidol-induced group, EEVC was treated for 21 days, and haloperidol (1 mg/kg) was administered to induce behavioural changes. Open-field, Y-Maze and traction tests were performed, and the mice brain acetylcholinesterase (AChE) enzyme was determined. Results: IC50 values in DPPH and ABTS assays were 85.5 μg/mL and 80 μg/mL, respectively and the total phenolic content of EEVC was found to be 0.166 mg. In a behavioral study, animals treated with 200 mg/kg and 400 mg/kg of EEVC exhibited a neuroprotective impact on AlCl3-induced neurodegeneration and haloperidol-induced behavioral changes with significant inhibition (P < 0.05 and P < 0.01, respectively) in acetylcholinesterase enzyme. Conclusion: The neuroprotection by EEVC postulated that it is a promising therapeutic agent for treating behavioral and cognitive dysfunctions. Further investigations on pro-inflammatory cytokine and neuroendocrine regulation in transgenic Alzheimer’s disease (AD)models complement the therapeutic value of V. corymbosum.

Effect of ethanolic extract of Centella asiatica on pentylene tetrazol induced seizure in albino mice

Background: Various preparations of the plant Centella asiatica were used in traditional medicine for treating memory disorders, insanity, epilepsy, headache, fever and dysentery. Hence this study was conducted to test the effect of Centella asiatica on classical animal model of epilepsy.Methods: First the ethanolic extract of Centella asiatica was subjected to acute toxicity study. Intraperitoneal injection of pentylene tetrazol in albino mice produces seizure. Plant extract was evaluated for protection from these experimental seizures. Four groups of animals were given the extract orally at 100mg, 200mg, 500mg and 1000mg per kilogram body weight. One group received phenobarbitone as standard drug and another group received distilled water as control. Time of onset of clonus is the study parameter. Statistical analysis of data was done using analysis of variance followed by Dunnet's test.Results: Various doses of plant extract ranging from 100mg to 1000mg/kg exhibited protection from experimentally induced seizures. Compared to control, the plant extract showed statistically significant delay in time of onset of clonus.Conclusions: Centella asiatica is potential source of anti-epileptic drug. Detailed phytochemical studies and animal experiments are recommended.

Stimulation of the Posterior Cingulate Cortex Impairs Episodic Memory Encoding.

Neuroimaging experiments implicate the posterior cingulate cortex (PCC) in episodic memory processing, making it a potential target for responsive neuromodulation strategies outside of the hippocampal network. However, causal evidence for the role that PCC plays in memory encoding is lacking. In human female and male participants (N = 17) undergoing seizure mapping, we investigated functional properties of the PCC using deep brain stimulation (DBS) and stereotactic electroencephalography. We used a verbal free recall paradigm in which the PCC was stimulated during presentation of half of the study lists, whereas no stimulation was applied during presentation of the remaining lists. We investigated whether stimulation affected memory and modulated hippocampal activity. Results revealed four main findings. First, stimulation during episodic memory encoding impaired subsequent free recall, predominantly for items presented early in the study lists. Second, PCC stimulation increased hippocampal gamma-band power. Third, stimulation-induced hippocampal gamma power predicted the magnitude of memory impairment. Fourth, functional connectivity between the hippocampus and PCC predicted the strength of the stimulation effect on memory. Our findings offer causal evidence implicating the PCC in episodic memory encoding. Importantly, the results indicate that stimulation targeted outside of the temporal lobe can modulate hippocampal activity and impact behavior. Furthermore, measures of connectivity between brain regions within a functional network can be informative in predicting behavioral effects of stimulation. Our findings have significant implications for developing therapies to treat memory disorders and cognitive impairment using DBS.SIGNIFICANCE STATEMENT Cognitive impairment and memory loss are critical public health challenges. Deep brain stimulation (DBS) is a promising tool for developing strategies to ameliorate memory disorders by targeting brain regions involved in mnemonic processing. Using DBS, our study sheds light on the lesser-known role of the posterior cingulate cortex (PCC) in memory encoding. Stimulating the PCC during encoding impairs subsequent recall memory. The degree of impairment is predicted by stimulation-induced hippocampal gamma oscillations and functional connectivity between PCC and hippocampus. Our findings provide the first causal evidence implicating PCC in memory encoding and highlight the PCC as a favorable target for neuromodulation strategies using a priori connectivity measures to predict stimulation effects. This has significant implications for developing therapies for memory diseases.

Dopamine is a double-edged sword: dopaminergic modulation enhances memory retrieval performance but impairs metacognition.

While memory encoding and consolidation processes have been linked with dopaminergic signaling for a long time, the role of dopamine in episodic memory retrieval remained mostly unexplored. Based on previous observations of striatal activity during memory retrieval, we used pharmacological functional magnetic resonance imaging to investigate the effects of dopamine on retrieval performance and metacognitive memory confidence in healthy humans. Dopaminergic modulation by the D2 antagonist haloperidol administered acutely during the retrieval phase improved recognition accuracy of previously learned pictures significantly and was associated with increased activity in the substantia nigra/ventral tegmental area, locus coeruleus, hippocampus, and amygdala during retrieval. In contrast, confidence for new decisions was impaired by unsystematically increased activity of the striatum across confidence levels and restricted range of responsiveness in frontostriatal networks under haloperidol. These findings offer new insights into the mechanisms underlying memory retrieval and metacognition and provide a broader perspective on the presence of memory problems in dopamine-related diseases and the treatment of memory disorders.

Effects of the active constituents of Crocus sativus L. crocins and their combination with memantine on recognition memory in rats.

Crocus sativus L., is a plant cultivated in many countries of the world. Crocins are among the active constituents of C. sativus and their implication in cognition has been proposed. The present study was designed to investigate in the rat the effects of crocins on distinct recognition memory components (encoding, storage and retrieval). Subsequently, the potential use of crocins as adjunctive agents for the treatment of memory disorders was examined. Thus, the effects exerted by a combination of subthreshold doses of crocins and memantine on recognition memory were evaluated. To assess the effects of compounds on memory, the novel object-recognition task (NORT) was used. In a preliminary study, the influence of the retention time (the delay between the two trials) on the performance of rats was assessed. Rats' recognition memory abilities remained intact up to 6 h, but were extinguished when a delay of 24 h was utilized. Crocins, at any dose tested (5, 15, and 30 mg/kg), did not affect rats' performance, whereas administration of higher doses (15 and 30 mg/kg) reversed delay-dependent deficits in the NORT. The combination of subthreshold doses of crocins (5 mg/kg) and memantine (3 mg/kg) did not influence the performance, but counteracted delay-dependent deficits in the NORT. These findings suggest that crocins counteract natural forgetting and may modulate different aspects of recognition memory, and that the combined use of crocins and memantine might represent a novel strategy to treat memory disorders.

Inhibition of AMPAR endocytosis alleviates pentobarbital-induced spatial memory deficits and synaptic depression

Our previous study has shown that pentobarbital causes memory deficits and impairs hippocampal synaptic plasticity. The Tat-GluA23Y peptide (GluA23Y) prevents activity-dependent α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) endocytosis. It enables early-phase long-term potentiation (LTP) to proceed to late-phase LTP allowing short-term memory to convert to long-term memory. The purpose of this study is to explore the potential effects of GluA23Y on pentobarbital-induced memory deficits through behavioral and electrophysiological paradigms. We found that in vivo intrahippocampal infusion of GluA23Y (100μM, 1μl per hippocampus) 30min prior to pentobarbital administration (8mM, 1μl per hippocampus) significantly rescued the pentobarbital-induced deficit of memory retrieval in rats during the Morris water maze test. Pre-incubation of GluA23Y (10μM) partially rescued bath application of pentobarbital-induced synaptic transmission of the CA3-CA1 pathway in hippocampal slices. More importantly, GluA23Y selectively upregulated the synaptic GluA2 expression that was suppressed by pentobarbital. Together, these results suggest that inhibition of GluA2-containing AMPAR endocytosis by GluA23Y increases the pentobarbital-suppressed basal synaptic transmission by upregulating the synaptic GluA2, and then subsequently alleviates spatial memory deficits. Therefore, inhibition of AMPAR endocytosis may be a potential therapeutic way to treat memory disorders caused by anesthetics.

Clinical effect of electroencephalographic biofeedback therapy in treatment of memory disorders in patients with acute severe toxic encephalopathy

Objective: To investigate the clinical effect and safety of electroencephalographic biofeedback therapy in improving memory disorders in patientsin the recovery stage of acute severe toxic encephalopathy. Methods: A total of 52 patients in the recovery stage of acute severe toxic encephalopathy who were hospitalized in our hospital from March 2013 to December 2016 were enrolled and randomly divided into observation group with 27 patients and control group with 25 patients. Both groups were given the drugs to promote the metabolism of brain cells,and the patients in the observation group were given electroencephalographic biofeedback therapy in addition. The Chinese revised version of Wechsler Memory Scale Type A was used to measure memory ability before and after each course of treatment. The treatment outcome was evaluated for both groups. Results: There were no significant differences in the scores of long-term memory,short-term memory, immediate memory, and memory quotient between the two groups before treatment(P>0.05).After the first course of treatment ended, the observation group had significant increases in the scores of forward task,backward task,association,and memory quotient(P<0.05); compared with the control group, the observation group had a significant reduction in the score of backward task(P<0.05).After the second course of treatmentended, the observation group had significant increases in the scores offorward task,backward task,memorization of pictures,reproduction,association,comprehension,and memory quotient,and the control group had significant increases in the scores of reproduction,association,comprehension,and memory quotient(P<0.05); compared with the control group, the observation group had significant increases in the scores of forward task,backward task,memorization of pictures, reproduction, association, comprehension, and memory quotient(P<0.05).Two patients experiencedchest distress, palpitation, and dysphoria during treatment, which did not affect the treatment. Conclusion: Electroencephalographic biofeedback therapy has a certain effect in the treatment of memory disorders in patients with acute severe toxic encephalopathy.

Screening of plants used in the European traditional medicine to treat memory disorders for acetylcholinesterase inhibitory activity and anti amyloidogenic activity

Ethnopharmacological relevancePlants used in the traditional medicine of Europe to treat memory dysfunction and/or to enhance memory were investigated for activity against the underlying mechanisms of Alzheimer's disease. Aim of the studyTo investigate 35 ethanolic extracts of plants, selected using an ethnopharmacological approach, for anti-amyloidogenic activity as well as an ability to inhibit the enzymatic activity of acetylcholinesterase. Materials and methodsThe anti-amyloidogenic activity of the extracts against amyloid beta was investigated by Thioflavin T fibrillation assays and the ability to inhibit the enzymatic activity of acetylcholinesterase was evaluated monitoring the hydrolysis of acetylthiocholine ResultsUnder the experimental conditions investigated, extracts of two plants, Carum carvi and Olea sylvestris, inhibited amyloid beta fibrillation considerably, eight plant extracts inhibited amyloid beta fibrillation to some extent, 16 plant extracts had no effect on amyloid beta fibrillation and nine extracts accelerated fibrillation of amyloid beta. Furthermore, five plant extracts from Corydalis species inhibited the enzymatic activity of acetylcholinesterase considerably, one plant extract inhibited the enzymatic activity of acetylcholinesterase to some extent and 29 plant extract had no effect on the enzymatic activity of acetylcholinesterase. ConclusionsAn optimal extract in this study would possess acetylcholinesterase inhibitory activity as well as anti-amyloidogenic activity in order to address multiple facets of Alzheimer's disease, until the molecular origin of the disease is unraveled. Unfortunately no such extract was found.

Establishing Natural Nootropics: Recent Molecular Enhancement Influenced by Natural Nootropic.

Nootropics or smart drugs are well-known compounds or supplements that enhance the cognitive performance. They work by increasing the mental function such as memory, creativity, motivation, and attention. Recent researches were focused on establishing a new potential nootropic derived from synthetic and natural products. The influence of nootropic in the brain has been studied widely. The nootropic affects the brain performances through number of mechanisms or pathways, for example, dopaminergic pathway. Previous researches have reported the influence of nootropics on treating memory disorders, such as Alzheimer's, Parkinson's, and Huntington's diseases. Those disorders are observed to impair the same pathways of the nootropics. Thus, recent established nootropics are designed sensitively and effectively towards the pathways. Natural nootropics such as Ginkgo biloba have been widely studied to support the beneficial effects of the compounds. Present review is concentrated on the main pathways, namely, dopaminergic and cholinergic system, and the involvement of amyloid precursor protein and secondary messenger in improving the cognitive performance.

The Contribution of Spatial and Temporal Molecular Networks in the Induction of Long-term Memory and Its Underlying Synaptic Plasticity.

The ability to form long-lasting memories is critical to survival and thus is highly conserved across the animal kingdom. By virtue of its complexity, this same ability is vulnerable to disruption by a wide variety of neuronal traumas and pathologies. To identify effective therapies with which to treat memory disorders, it is critical to have a clear understanding of the cellular and molecular mechanisms which subserve normal learning and memory. A significant challenge to achieving this level of understanding is posed by the wide range of distinct temporal and spatial profiles of molecular signaling induced by learning-related stimuli. In this review we propose that a useful framework within which to address this challenge is to view the molecular foundation of long-lasting plasticity as composed of unique spatial and temporal molecular networks that mediate signaling both within neurons (such as via kinase signaling) as well as between neurons (such as via growth factor signaling). We propose that evaluating how cells integrate and interpret these concurrent and interacting molecular networks has the potential to significantly advance our understanding of the mechanisms underlying learning and memory formation.

In Vivo Anti-Hyperglycemic Potential of Brahmi Gritham and Docking Studies of Its Active Components Against Protein Kinase C and CD38

The anti-hyperglycemic and antioxidant effects of the Indian herbal formulation Brahmi gritham were studied in streptozotocin-induced diabetic female Wistar albino rats. Diabetes was induced by a single dose of streptozotocin (55 mg/kg body weight [b.w.], i.p.). Estimation of blood glucose levels, liver glycogen content and antioxidant levels were carried out in experimental rats. The tested parameters were compared with those of the glibenclamide (600 μg/kg b.w.) treated group. Molecular docking studies were carried out to analyze the interaction patterns of protein kinase C (PKC) and CD38 of chosen proteins of signal transduction pathways that are significant in the pathogenesis of diabetes against active components of Brahmi gritham. Immunohistochemistry of pancreas revealed that Brahmi gritham was able to restore β-cell mass and function near to that of the normal control. In silico studies showed that apigenin and quercetin showed significant interactions with PKC, while clitorin, bacopaside I and II showed significant interactions with CD38. Quercetin showed highest percentage inhibition of α-amylase enzyme. Practical Applications Brahmi gritham is a traditional polyherbal formulation used in Ayurveda to treat memory disorders. The individual components of this formulation are known to possess significant antioxidant properties and contain several biologically active compounds found to be effective in treating various disorders, including diabetes and obesity. The efficacy of Brahmi gritham in diabetes management has not yet been studied, and therefore, the present study provides insights into the anti-hyperglycemic potential of this formulation in rat model. In addition, the results of in silico analysis would pave way for better utilization of the flavonoids quercetin and apigenin in diabetes management and in particular microvascular diabetic complications.

Ambulatory Care for Dementia in Switzerland: Results of a Nationwide Survey

Background The early and correct identification and treatment of memory disorders is crucial for the well-being and prognosis of persons with dementia and their families. Family physicians are in the key position, but previous surveys showed, that their competency regarding this task is too low, although they regard dementia diagnosis as part of their job. Method After a pilot study with personal interviews we designed a web-based survey. It presented case vignettes, case 1 with mild cognitive impairment in a male or female version, case 2 describing a moderate dementia syndrome in a female multimorbid person. Three alternatives described a typical course of vascular dementia, Alzheimer dementia and Lewy Body dementia. One version of case 1 and case 2 each were randomized to the participants. The questionnaire consisted of open questions and those with given answer categories. Results From 7‘603 invitations and additional reminders, we received 709 full answers (9.3%). The physicians were family physicians (50.7%), specialists for internal medicine (23.2%), psychiatrists (21.9%) and neurologists (3.5%). The respondents were representative regarding age and sex distribution for swiss physicians. Regarding diagnosis, a vascular concept of memory disorders is still strong. Alzheimer dementia is still considered by a low number of physicians. For the investigations neuropsychological screening tests were cited frequently, neuroimaging less often. Antidementia drugs were considered in about 60% of case 1 and less frequently in case 2. Non-drug approaches covered a wide range of activities and were mentioned by two thirds of the physicians. Conclusion Compared to previous surveys using other methods we detect some improvement in guideline adherence. However there still remains much to do to improve medical outpatient care. We thank the Swiss Alzheimer Associaton for funding this study.

TRPC3 channels critically regulate hippocampal excitability and contextual fear memory

Memory formation requires de novo protein synthesis, and memory disorders may result from misregulated synthesis of critical proteins that remain largely unidentified. Plasma membrane ion channels and receptors are likely candidates given their role in regulating neuron excitability, a candidate memory mechanism. Here we conduct targeted molecular monitoring and quantitation of hippocampal plasma membrane proteins from mice with intact or impaired contextual fear memory to identify putative candidates. Here we report contextual fear memory deficits correspond to increased Trpc3 gene and protein expression, and demonstrate TRPC3 regulates hippocampal neuron excitability associated with memory function. These data provide a mechanistic explanation for enhanced contextual fear memory reported herein following knockdown of TRPC3 in hippocampus. Collectively, TRPC3 modulates memory and may be a feasible target to enhance memory and treat memory disorders.

Validated HPLC-DAD method for stability study of sulbutiamine HCl

Sulbutiamine (SUL) is a synthetic thiamine derivative widely used for treatment of memory disorders.

Efficacy of Cortexin in the Treatment of Memory Disorders in Children

Children, aged from 7 to 12 years, with memory disorders were treated with cortexin (30 patients) and encephabol (30 patients). The comparative evaluation of efficacy and safety of these drugs was carried out. The higher cortexin efficacy (the improvement in 86.7% of cases) in comparison with encephabol (the improvement in 63.3% of cases) confirmed by the data of neuropsychological and neurophysiological research is established.