Tag Archive: Cerebrolysin


Abstract
Cerebrolysin is a drug consisting of low-molecular-weight neurotrophic peptides and free amino acids. Cerebrolysin has been shown to ameliorate the effects of oxidative stress, reduce apoptosis, and promote neuronal growth in several degenerative and acquired central nervous system insults, including dementias, stroke, and traumatic injuries. Little is known about its therapeutic efficacy in peripheral nervous system diseases. In this study, we clinically evaluated the effects of cerebrolysin on peripheral nervous system lesions. We evaluated the clinical efficacy of cerebrolysin in six patients with the following conditions who failed to respond to conventional therapies: (1) atonic bladder due to inflammatory radiculitis; (2) paraplegia due to inflammatory radiculoneuropathy; (3) post-traumatic brachial plexopathy; (4) compressive radial nerve injury; (5) post-traumatic facial nerve paralysis; and (6) diabetic ophthalmoplegia. Our results showed that cerebrolysin was more associated with rapid neurological recovery after various peripheral nerve lesions than other therapies including steroids and supportive therapies such as vitamins and antioxidants. The present results support the therapeutic efficacy of cerebrolysin in the treatment of acquired peripheral nervous system diseases.
Key Words: cerebrolysin; neurotrophic effect; neuroprotection; peripheral nervous system

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Cerebrolysin in dementia treatment

Cerebrolysin: a review of its use in dementia

Source

Adis, a Wolters Kluwer Business, Auckland, New Zealand. demail@adis.co.nz

Abstract

Cerebrolysin is a parenterally administered, porcine brain-derived peptide preparation that has pharmacodynamic properties similar to those of endogenous neurotrophic factors. In several randomized, double-blind trials of up to 28 weeks’ duration in patients with Alzheimer’s disease, Cerebrolysin was superior to placebo in improving global outcome measures and cognitive ability. A large, randomized comparison of Cerebrolysin, donepezil or combination therapy showed beneficial effects on global measures and cognition for all three treatment groups compared with baseline. Although not as extensively studied in patients with vascular dementia, Cerebrolysin has also shown beneficial effects on global measures and cognition in this patient population. Cerebrolysin was generally well tolerated in clinical trials, with dizziness (or vertigo) being the most frequently reported adverse event. Although further studies with Cerebrolysin, including longer term trials and further exploration of its use in combination with cholinesterase inhibitors, are needed to more clearly determine its place in the management of Alzheimer’s disease and vascular dementia, available data suggest that Cerebrolysin is a useful addition to the treatment options available for dementia.

PMID:
19848437
[PubMed - indexed for MEDLINE]

BUY CEREBROLYSIN AMPS HERE

Abstract

To determine the therapeutic effect of nootropic agent Cerebrolysin on patients with mild to moderate Alzheimer’s disease (AD), we searched the Cochrane Library, Medline, PubMed, and Chinese Biomedical Literature Analysis and Retrieval System for Compact Disc (CBMDISC), and communicated with EBEWE Pharmaceutical Ltd, for randomized trials comparing Cerebrolysin with placebo in AD. Available data on clinical global impression, cognitive performance and activities of daily living were extracted from 6 randomized double-blind placebo-controlled clinical trials and combined with standard meta-analysis methods. An infusion with Cerebrolysin for 4 weeks (30 ml Cerebrolysin daily on five consecutive days of each week) led to a significant improvement of the clinical global impression. Compared with placebo, log(OR) was 1.1799, and 95% confident interval was 0.7463-1.6135 (P < 0.05), indicating that Cerebrolysin could significantly improve the clinical global impression in patients with mild to moderate AD. However, more convincing evidences are needed for the efficacy of Cerebrolysin on the cognitive performance and activities of daily living.

PMID:
17318304
[PubMed - indexed for MEDLINE]

A 24-week, double-blind, placebo-controlled study of three dosages of Cerebrolysin in patients with mild to moderate Alzheimer’s disease

Source

Euroespes Biomedical Research Centre, Santa Maria de Babio, Bergondo, La Coruna, Spain. xantonal@yahoo.es

Abstract

Cerebrolysin (Cere) is a compound with neurotrophic activity shown to be effective in Alzheimer’s disease in earlier trials. The efficacy and safety of three dosages of Cere were investigated in this randomized, double-blind, placebo-controlled, study. Two hundred and seventy-nine patients were enrolled (69 Cere 10 ml; 70 Cere 30 ml; 71 Cere 60 ml and 69 placebo). Patients received iv infusions of 10, 30, 60 ml Cere or placebo 5 days/week for the first 4 weeks and thereafter, two iv infusions per week for 8 weeks. Effects on cognition and clinical global impressions were evaluated 4, 12 and 24 weeks after the beginning of the infusions using the CIBIC+ and the modified Alzheimer’s Disease Assessment Scale (ADAS)-cog. At week 24, significant improvement of cognitive performance on the ADAS-cog (P=0.038) and global function (CIBIC+; P>0.001) was observed for the 10 ml dose. The 30 and 60 ml doses showed significant improvement of the global outcome but failed to show significant improvement of cognition. The results are consistent with a reversed U-shaped dose-response relationship for Cere. The percentage of patients reporting adverse events was similar across all study groups. Cere treatment was well tolerated and led to significant, dose-dependent improvement of cognition and global clinical impression.

PMID:
16420392
[PubMed - indexed for MEDLINE]

The neuroprotective effects of Cerebrolysin in a transgenic model of Alzheimer’s disease are associated with improved behavioral performance

Source

Department of Neurosciences, University of California San Diego, School of Medicine, La Jolla, CA 92093, USA.

Abstract

Cerebrolysin is a peptide mixture with neurotrophic effects that might have the ability of both reducing amyloid burden and improving synaptic plasticity in Alzheimer’s disease (AD). In order to determine if Cerebrolysin is capable of ameliorating the neurodegenerative and behavioral alterations associated with amyloid beta (A beta) production; transgenic (tg) mice expressing mutant human amyloid precursor protein (APP) under the Thy1 promoter were treated with Cerebrolysin or saline alone starting at 3 or 6 months of age for a total of three months. Animals were then tested behaviorally (at 6 and 9 months of age respectively) in the water maze and then analyzed neuropathologically for amyloid burden, synaptic density, astrogliosis and apoptosis. Performance analysis in the water maze showed that in the younger tg mice cohort, Cerebrolysin treatment significantly ameliorated the performance deficits. In the older cohort, there was a trend toward improved performance in the learning curve. Neuropathological examination showed that in both age/treatment groups, Cerebrolysin promoted synaptic regeneration, and reduced the proportion of neurons displaying DNA fragmentation by the (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL) method. Moreover, Cerebrolysin treatment reduced A beta burden by 43% in the young group and by 27% in the older group. Taken together, these results suggest that Cerebrolysin treatment might have beneficial effects in patients with cognitive impairment by reducing A beta accumulation and promoting the preservation of synaptic terminals.

PMID:
14628195
[PubMed - indexed for MEDLINE]

Improved global function and activities of daily living in patients with AD: a placebo-controlled clinical study with the neurotrophic agent Cerebrolysin.

Source

Neurology Department, University of Cluj-Napoca, Cluj-Napoca, Romania.

Abstract

BACKGROUND:

Cerebrolysin (Cere) is a peptidergic, neurotrophic drug which has been shown to improve cognitive performance and global function of Alzheimer’s disease (AD) patients in earlier trials. In this study, we have attempted to replicate this findings with particular emphasis on functional improvement of the patients.

PATIENTS AND METHODS:

Patients received infusions of 30 ml Cere or placebo five days/week for six consecutive weeks. Patients had to have a diagnosis of AD and a MMSE score of 14-25 inclusive. Effects on cognition, global function, and activities of daily living were evaluated 3, 6, and 18 weeks after the beginning of the infusions.

RESULTS:

Significant improvement of cognitive function, clinical global impression and activities of daily living were seen after the end of the therapy. The effects were most pronounced in the DAD score, a measure for the capability to perform activities of daily living. Interestingly, and in line with the findings of earlier studies, the treatment effect of Cere was maintained after cessation of treatment up to the week 18 assessment.

CONCLUSION:

The data confirm the findings of earlier trials and clearly demonstrates that Cere leads to functional improvement of patients with AD. The sustained treatment effect of Cere after withdrawal has been confirmed.

PMID:
12456070
[PubMed - indexed for MEDLINE]

Neuro-enhancement – Brain doping

Source

Klinik und Poliklinik für Psychiatrie und Psychotherapie, Ismaningerstr. 22, 81675, München. hans.foerstl@lrz.tu-muenchen.de

Abstract

Cognitive enhancement, the increase in the mental ability by psychoactive substances and other interventions has received a renewed boost through the development of innovative principle. More than 100 drugs are currently being developed, tested or used for cognitive enhancement. Cholinesterase inhibitors, memantine, dimebon, ampakines, fluoxetine and other antidepressants, methylphenidate and modafinil are candidates awaiting a larger distribution as cognitive enhancers in healthy individuals, if their advantages can be demonstrated. Beyond more general neuro-ethical reservations regarding neuro-enhancement, future research will need to address the following neuropsychiatric issues: (1) will the benefits of longer term neuro-enhancement outweigh potential disadvantages such as rebound effects and other neurobiological and psychosocial trade-offs? (2) What will be the neuropsychiatric sequelae of a soft coercion towards drug usage at work and for recreational purposes? (3) Will there be new and specific neuropsychiatric diseases due to long-term usage of neuro-enhancers in a larger population? Novel strategies of neuro-enhancement will have to demonstrate their superiority compared with more traditional and well-established interventions such as coffee and cake.

PMID:
19565292
[PubMed - indexed for MEDLINE]

Cognition enhancers between treating and doping the mind

Source

Department of Experimental and Applied Pharmacology, Centre of Excellence in Applied Biology, University of Pavia, Viale Taramelli 14, 27100 Pavia, Italy.

Abstract

Memory, attention and creativity represent three different cognitive domains, which are interconnected and contribute the “mental performance” of an individual. Modern neuroscience has investigated some of the neuronal circuits and of the neurotransmitters and molecular events underlying the above-mentioned cognitive functions. Within this renewed reference context, some of the properties of the components of the remedies to increase mental performance have been studied and validated in experimental models and, to date, these substances are named “smart drugs”, “memory enhancing drugs” or “nootropic drugs” (from the Greek root noos for mind and tropein for toward). Recently pharmaceutical industries are increasingly focusing on the research for potential substances in this field: several “smart drugs” are in clinical trials and could be on the market in few years. Furthermore, a quick survey from Internet highlights the presence of a great variety of both approved and non-approved drugs, with some of them addressing to only medical and others to performance-oriented use, opening room to some reflections or speculations from scientific and ethical points of view. In order to point out the effect of nootropic drugs on cognition of healthy people, we reviewed the literature on drug enhancement of various cognitive functions, including memory, attention and creativity. As their simplest, memory is regarded as the ability to remember events or learned material, attention is the cognitive process of selectively concentrating on one aspect while ignoring distracters and creativity could be described as the ability to create products or ideas which are original and which possess a social usefulness. Reports from literature reveal that some medications currently available to patients with memory disorders may also increase performances in healthy people and that drugs designed for psychiatric disorders can also be used to enhance certain mental functions. However, the long-term effects of these drugs are unknown, but their apparent effectiveness allows room to their use and misuse. At variance with these literature data showing scientific, even if poor, evidence of the effect of smart drugs in the field of memory and attention, only indirect information on creativity can be obtained by studies of the effects of diseases and drugs on the artistic productivity of classic painters and famous authors, offering a link to understand the neuronal basis of this cognitive function and a cue to understand how drugs (used to correct the illness) may affect the function. On the basis of these cues, in this review we will discuss some critical aspects of the different cerebral circuits and molecular events regulating memory, attention and creativity in order to outline the neurobiological bases of the effects of “smart drugs” on cognitive functions, and to evaluate their putative pharmaceutical development.

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Abstract

The therapeutic effect of Cerebrolysin in the treatment of dementia and brain injury has been proposed because of neurotrophic properties of this compound. Since an increased kynurenine metabolism has been documented in several brain pathologies including dementia the aim of the present study was to investigate the biochemical properties of Cerebrolysin with respect to kynurenic acid (KYNA) formation in an in vitro study. KYNA is an endogenous metabolite of the kynurenine pathway of tryptophan degradation and is an antagonist of the glutamate ionotropic excitatory amino acid and of the nicotine cholinergic receptors. The activities of the KYNA synthesizing enzymes kynurenine aminotransferases I, II and III (KAT I, KAT II and KAT III) in rat liver, and rat and human brain homogenates were analysed in the presence of Cerebrolysin. KAT I, II and III activities were measured using a radio-enzymatic method in the presence of 1 mM pyruvate and 100 µM [H3]l-kynurenine. Cerebrolysin, dose-dependently and significantly reduced KAT I, KAT II and KAT III activities of rat liver homogenate. Furthermore, Cerebrolysin exerted a dose-dependent inhibition of rat and human brain KAT I, KAT II and KAT III activities, too. The inhibitory effect of Cerebrolysin was more pronounced for KAT I than for KAT II and KAT III. The present study for the first time demonstrates the ability of Cerebrolysin to lower KYNA formation in rat liver as well as in rat and human brain homogenates. We propose Cerebrolysin as a compound susceptible of therapeutic exploitation in some disorders associated with elevated KYNA metabolism in the brain and/or other tissues. We suggest that the anti-dementia effect of Cerebrolysin observed in Alzheimer patients could be in part due to Cerebrolysin induced reduction of KYNA levels, thus modulating the cholinergic and glutamatergic neurotransmissions.

Abbreviations: KYNA, kynurenic acid, KAT, kynurenine aminotransferase, NMDA, N-methyl-d-aspartate, EAA, excitatory amino acid, CNS, central nervous system

Keywords: Kynurenic acid, Kynurenine aminotransferases, NMDA receptor, Cholinergic receptor, Dementia, Cerebrolysin

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