17 research outputs found
The gag proteins of human immunodeficiency virus type 1: mechanisms of virus assembly and possibilities for interference
Neurofunctional consequences of developmental exposure to moderate doses of cannabinoids in a rat model
Effect of Maharishi Amrit Kalash on Age Dependent Variations in Mitochondrial Antioxidant Enzymes, Lipid Peroxidation and Mitochondrial Population in Different Regions of the Central Nervous System of Guinea-pigs
Apical vulnerability to dendritic retraction in prefrontal neurones of ageing SAMP10 mouse: a model of cerebral degeneration
Length Changes in Dendritic Networks of Cerebellar Purkinje Cells of Old Rats after Chronic Ethanol Treatment
Spatial Discrimination and Passive Avoidance Behavior in The Rat: Age-Related Changes and Modulation by Chronic Dietary Choline Enrichment
Neuroprotective Properties of Glycosaminoglycans: Potential Treatment for Neurodegenerative Disorders
Previous studies suggest that proteoglycans and glycosaminoglycans (GAGs) may play an important role in the pathogenesis and/or alleviation of neurodegenerative disorders, including Alzheimer's disease (AD). Proteoglycans increase the formation of neurofibrillary tangles, and stimulate the aggregation of β-amyloid (Aβ). This effect, on the other hand, is believed to be competitively inhibited by certain GAGs. Over the past few years, we have examined the neuroprotective properties of Neuroparin (C3), a low-molecular-weight GAG (approx. 2.1 kDa), in animal models of lesions characteristic of AD. Neuroparin is composed of 4–10 oligosaccharides, and it is derived from heparin involving depolymerization of heparin by gamma irradiation. In our experiments, Neuroparin protected against cholinergic lesions induced by intracerebroventricular injection of a specific cholinotoxin, AF64A, in rats. Administration of Neuroparin attenuated AF64A-stimulated, low-affinity nerve growth factor receptor-immunoreactive axonal varicosities in the rat septum, and increased arborization of hippocampal CA1 neurons. Neuroparin also reduced the septal caspase 3 immunoreactivity induced by AF64A treatment. Moreover, Neuroparin reduced tau 2 immunoreactivity in the rat hippocampus, stimulated by intra-amygdaloid injection of Aβ25–35. These findings are in good agreement with our previous data indicating a neuroprotective role of GAGs. These results, plus others, all suggest that Neuroparin may possess neuroprotective properties against many of the characteristic neural lesions in AD. Since our pharmacokinetic studies revealed that Neuroparin is capable of crossing the blood-brain barrier, Neuroparin may, conceivably, open an entirely new avenue in the treatment of neurodegenerative disorders. Phase I studies have been completed, and have proven to be extremely supportive in that regard