The study tested the hypothesis that cerebrolysin protects the brain from free radicals in rats treated with 3-nitropropionic acid (3-NPA). To address this hypothesis, the levels of dopamine (DA) and some oxidative stress biomarkers were measured after ...
Calderón Guzmán David +8 more
doaj +1 more source
Chronic cerebral ischemia, neuroplasticity, possibilities of therapy
The paper presents current views on the pathogenetic mechanisms of cerebral ischemia. It discusses the role of neurotrophins in the processes of neuroplasticity. Experimental and clinical studies of the neuropeptide drug Cerebrolysin are reviewed.
E. I. Chukanova, A. S. Chukanova
doaj +1 more source
GSK3: A potential target and pending issues for treatment of Alzheimer's disease
GSK3 signaling in Alzheimer's disease and targeted therapies. Abstract Glycogen synthase kinase‐3 (GSK3), consisting of GSK3α and GSK3β subtypes, is a complex protein kinase that regulates numerous substrates. Research has observed increased GSK3 expression in the brains of Alzheimer's disease (AD) patients and models.
Jiahui Zhao +6 more
wiley +1 more source
Cerebrolysin Attenuates Heat Shock Protein (HSP 72 KD) Expression in the Rat Spinal Cord Following Morphine Dependence and Withdrawal: Possible New Therapy for Pain Management [PDF]
The possibility that pain perception and processing in the CNS results in cellular stress and may influence heat shock protein (HSP) expression was examined in a rat model of morphine dependence and withdrawal. Since activation of pain pathways result in
Ali, Syed F +5 more
core +2 more sources
The protective role of endothelial GLUT1 in ischemic stroke
Following the endocytosis, internalized membrane‐bound vesicles containing GLUT1 protein enter the early endosome (EE) to start sorting process. In EE, selected GLUT1 cargoes can be directly recycled to the membrane, termed “fast recycling”, or interact with trans‐Golgi network, termed “trans‐Golgi transport”.
Qiwei Peng, Weiqi Zeng
wiley +1 more source
Current evidence of synaptic dysfunction after stroke: Cellular and molecular mechanisms
Stroke can cause synaptic loss and dysfunction, reducing communication between neurons. Stroke is known to cause the death of neuronal and endothelial cells, trigger microglia and astrocyte activation, and lead to synaptic dysfunction. Abstract Background Stroke is an acute cerebrovascular disease in which brain tissue is damaged due to sudden ...
Chuan Li +9 more
wiley +1 more source
In vitro anti-cholinesterase and anti-oxidant activity of three standardised polyherbal products used for memory enhancing in ethnomedicine of South-East Nigeria [PDF]
Background: Polyherbal standardised extracts used in ethnomedicine of Eastern Nigeria for memory improvements were evaluated for anti-cholinesterases and anti-oxidant properties.
Carter, Wayne +2 more
core +2 more sources
Vascular dementia is one of the most common causes of dementia after Alzheimer's disease, causing around 15% of cases. However, unlike Alzheimer's disease, there are no licensed treatments for vascular dementia.
O'Brien, John T, Thomas, Alan
core
Alzheimer's disease phenotype based upon the carrier status of the apolipoprotein E ɛ4 allele
Genetic variation in the APOE genotype form the basis of the clinical phenotype. Abstract The apolipoprotein E ɛ4 allele (APOE4) is universally acknowledged as the most potent genetic risk factor for Alzheimer's disease (AD). APOE4 promotes the initiation and progression of AD. Although the underlying mechanisms are unclearly understood, differences in
Xiao‐Yu Ji +7 more
wiley +1 more source
Endogenous Kynurenine Aminotransferases Inhibitor is Proposed to Act as “Glia Depressing Factor” (GDF) [PDF]
The endogenous neuroinhibitory amino acid receptor antagonist kynurenic acid (KYNA) has been hypothetically linked to physiological processes and to the pathogenesis of several brain disorders.
Baran, Halina +2 more
core +3 more sources

