Effects of beta-amyloid on behavioral and amino acids spectrum in rats' brain and their modulation by embryonic proteins.
One of the crucial events in the pathogenesis of neurodegenerative disorders linked with dementia-like Alzheimer's Disease (AD) is the disturbance in neurotransmission based on progressive deficit of neuromediators that is manifested by marked decrease in cognitive behavior, loss of memory and inability to learn as a result of impairment in synaptic plasticity of neurons. In this study we have used a new complex of proteoglycans of embryonic genesis (PEG) created by Prof. L. Mkrtchyan, as a possible therapeutic approach that can rescue neurons from further degeneration caused by beta-amyloid (Abeta). We attempt to reveal the biochemical (determination of neuroactive amino acids such as glutamate, GABA, taurine, glycine and aspartate) changes and behavior on Y-maze and avoidance/exploratory activity on elevated plus-maze task in rats' brain after modeling Alzheimer's disease by i.c.v. injection of Abeta25-35. Furthermore, in this study we analyzed the neuroprotective properties of PEG. Under the influence of PEG the concentration of all investigated amino acids both in cerebral cortex and hippocampus (except striatum changes) increased. In the present study we demonstrated that bilateral i.c.v. injection of aggregated Abeta25-35 in dosage 30nmol/rat resulted in impairment in spatial alternation behavior. Both preliminary (single) and double injection of PEG showed constant improvement of spatial memory after the first trial up to 90 days after i.c.v. injection of aggregated Abeta25-35. Our findings suggest that proteoglycans of embryonic genesis in neurodegenerative state show an expressed regulatory-protective effect.
Yenkoyan
Konstantin
K
Department of Biochemistry, Yerevan State Medical University, Armenia. enkoyan@yahoo.com
Safaryan
Karen
K
Navasardyan
Griselda
G
Mkrtchyan
Levon
L
Aghajanov
Michael
M
D000596:Amino Acids / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000633:toxicity; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D001923:Brain Chemistry / Q000187:drug effects* / Q000502:physiology; D007839:Functional Laterality / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D008297:Male; D008569:Memory Disorders / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism; D018696:Neuroprotective Agents / Q000138:chemical synthesis / Q000494:pharmacology* / Q000627:therapeutic use; D010446:Peptide Fragments / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000633:toxicity; D011509:Proteoglycans / Q000138:chemical synthesis / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D013654:Taurine / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000596:Amino Acids; D016229:Amyloid beta-Peptides; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D011509:Proteoglycans; C074636:amyloid beta-protein (25-35); D013654:Taurine; D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D005998:Glycine