Amelioration of the cerebrovascular amyloidosis in a transgenic model of Alzheimer’s disease with the neurotrophic compound Cerebrolysin™

No abstract is available for this paper.

• Publication year

  2005

• Venue

  Journal of neural transmission

• Publication date

  2005-02-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/s00702-004-0181-4PMID 15657642
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Clinical manifestations of cerebral amyloid angiopathy–related inflammation

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• Caspase cleavage of the amyloid precursor protein modulates amyloid β‐protein toxicity

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• Amyloid beta protein toxicity mediated by the formation of amyloid-beta protein precursor complexes.

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• Matrix metalloproteinase–9 and spontaneous hemorrhage in an animal model of cerebral amyloid angiopathy

  2003cited by this paper
• Amyloid β protein toxicity mediated by the formation of amyloid‐β protein precursor complexes

  2003cited by this paper
• Cerebral amyloid angiopathy: Pathogenesis and effects on the ageing and Alzheimer brain

  2003cited by this paper
• Proteolytic processing of the Alzheimer's disease amyloid precursor protein in brain and platelets

  2003cited by this paper
• The neuroprotective effects of Cerebrolysin™ in a transgenic model of Alzheimer’s disease are associated with improved behavioral performance

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• Sporadic and Familial Cerebral Amyloid Angiopathies

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• Generation of C‐terminally truncated amyloid‐β peptides is dependent on γ‐secretase activity

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• Nerve inflammation halts trial for Alzheimer's drug

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• Effects of Cerebrolysin on amyloid-beta deposition in a transgenic model of Alzheimer's disease.

  2002cited by this paper
• Localization of a Fibrillar Amyloid β-Protein Binding Domain on Its Precursor*

  2002cited by this paper
• Generation of C-terminally truncated amyloid-beta peptides is dependent on gamma-secretase activity.

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• Macrophage/Microglia-specific Protein Iba1 Enhances Membrane Ruffling and Rac Activation via Phospholipase C-γ-dependent Pathway*

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• Localization of a fibrillar amyloid beta-protein binding domain on its precursor.

  2002cited by this paper
• Amplification of blood-brain barrier GLUT1 glucose transporter gene expression by brain-derived peptides.

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• A short cytoplasmic domain of the amyloid precursor protein induces apoptosis in vitro and in vivo.

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• Perturbed endoplasmic reticulum function, synaptic apoptosis and the pathogenesis of Alzheimer's disease.

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• Spontaneous Hemorrhagic Stroke in a Mouse Model of Cerebral Amyloid Angiopathy

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• Early formation of mature amyloid‐β protein deposits in a mutant APP transgenic model depends on levels of Aβ1–42

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• Chronic overproduction of transforming growth factor-beta1 by astrocytes promotes Alzheimer's disease-like microvascular degeneration in transgenic mice.

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• High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation

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• Genetically altered transgenic models of Alzheimer's disease.

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• Prominent cerebral amyloid angiopathy in transgenic mice overexpressing the london mutant of human APP in neurons.

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• Neurotrophic effects of Cerebrolysin in animal models of excitotoxicity.

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• Apoptotic and Anti‐Apoptotic Synaptic Signaling Mechanisms

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• In vitro synaptotrophic effects of Cerebrolysin in NT2N cells

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• Cerebrolysin ameliorates performance deficits, and neuronal damage in apolipoprotein E-deficient mice.

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• In vivo upregulation of the blood-brain barrier GLUT1 glucose transporter by brain-derived peptides.

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• Brain-derived peptides reduce the size of cerebral infarction and loss of MAP2 immunoreactivity after focal ischemia in rats.

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• Amyloidogenic role of cytokine TGF-β1 in transgenic mice and in Alzheimer's disease

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• Brain-derived peptides increase the expression of a blood-brain barrier GLUT1 glucose transporter reporter gene.

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• Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

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• Levels and Alternative Splicing of Amyloid β Protein Precursor (APP) Transcripts in Brains of APP Transgenic Mice and Humans with Alzheimer's Disease (*)

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• Brain-derived peptides regulate the steady state levels and increase stability of the blood-brain barrier GLUT1 glucose transporter mRNA.

  1995cited by this paper
• Efficacy of the Peptidergic Nootropic Drug Cerebrolysin in Patients with Senile Dementia of the Alzheimer Type (SDAT)

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• Cleavage at the N-terminal site of Alzheimer amyloid beta/A4 protein is essential for its secretion.

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• Efficacy of Cerebrolysin® in Alzheimer’s disease

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• Glucose Deprivation Causes Posttranscriptional Enhancement of Brain Capillary Endothelial Glucose Transporter Gene Expression via GLUT1 mRNA Stabilization

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• Importance of Modulating Kynurenic Acid Metabolism—Approaches for the Treatment of Dementia

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• CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer’s disease

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• Pathological changes within the cerebral vasculature in Alzheimer’s disease: New perspectives

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• Superior antioxidant and anti-ischemic neuroprotective effects of cerebrolysin in heat stroke following intoxication of engineered metal Ag and Cu nanoparticles: A comparative biochemical and physiological study with other stroke therapies.

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• Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

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• Cerebrolysin in the therapy of mild cognitive impairment and dementia due to Alzheimer's disease: 30 years of clinical use

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• Review of Alterations in Perlecan-Associated Vascular Risk Factors in Dementia

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• The extracellular matrix of the blood–brain barrier: structural and functional roles in health, aging, and Alzheimer’s disease

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• Effect of cerebrolysin on gross motor function of children with cerebral palsy: a clinical trial

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• Effects of Various Kynurenine Metabolites on Respiratory Parameters of Rat Brain, Liver and Heart Mitochondria

  2016cites this paper
• Neuro-peptide treatment with Cerebrolysin improves the survival of neural stem cell grafts in an APP transgenic model of Alzheimer disease.

  2015cites this paper
• Neuropeptide Treatment with Cerebrolysin Enhances the Survival of Grafted Neural Stem Cell in an α-Synuclein Transgenic Model of Parkinson’s Disease

  2015cites this paper
• Neuroprotective effects of Cerebrolysin in triple repeat Tau transgenic model of Pick’s disease and fronto-temporal tauopathies

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• Enhanced Aβ1–40 Production in Endothelial Cells Stimulated with Fibrillar Aβ1–42

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• Regional Comparison of the Neurogenic Effects of CNTF-Derived Peptides and Cerebrolysin in AβPP Transgenic Mice

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• Increased CDK5 expression in HIV encephalitis contributes to neurodegeneration via tau phosphorylation and is reversed with Roscovitine.

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• The chronic administration of cerebrolysin induces plastic changes in the prefrontal cortex and dentate gyrus in aged mice

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• Beneficial effects of a neurotrophic peptidergic mixture persist for a prolonged period following treatment interruption in a transgenic model of Alzheimer's disease

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• Endogenous Kynurenine Aminotransferases Inhibitor is Proposed to Act as “Glia Depressing Factor” (GDF)

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• Deletion of the α7 Nicotinic Acetylcholine Receptor Gene Improves Cognitive Deficits and Synaptic Pathology in a Mouse Model of Alzheimer's Disease

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• Neurofibrillary and neurodegenerative pathology in APP-transgenic mice injected with AAV2-mutant TAU: neuroprotective effects of Cerebrolysin

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