Neuroprotection by hypothalamic peptide proline-rich peptide-1 in Aβ25–35 model of Alzheimer's disease

@article{Galoyan2008NeuroprotectionBH,
  title={Neuroprotection by hypothalamic peptide proline-rich peptide-1 in A$\beta$25–35 model of Alzheimer's disease},
  author={Armen A. Galoyan and John S. Sarkissian and Vergine A. Chavushyan and Irina B. Meliksetyan and Zaruhi E. Avagyan and M. V. Poghosyan and Hasmik G. Vahradyan and Hovhannes H. Mkrtchian and Davit O. Abrahamyan},
  journal={Alzheimer's \& Dementia},
  year={2008},
  volume={4},
  pages={332-344}
}
The proline-rich hypothalamic peptide is a modulator of functions of neurotrophins and neuronal activity in amyloid-induced neurodegeneration
TLDR
Electrophysiological and morphological studies of hippocampal neurons show, that by the 18th week after the beginning of neuro-degeneration, treatment with PRP-1 results in survival and further maintenance of cells, which indicates that PRp-1 has neuroprotective characteristics.
The role of monoamines in the development of Alzheimer's disease and neuroprotective effect of a proline rich polypeptide
NEW MECHANISMS OF NEUROHORMONAL REGULATION UNDER CONDITIONS OF NEURODEGENERATION
TLDR
The results of recent research work allowed us to fulfill the present conception about multiform expressions of high biological activity of PRP and convincingly to demonstrate the existence of its central and peripheral immunomodulating action, the ability to regulate the brain free radical processes, the level of lipid peroxidation and as a whole to prevent and correlate the brain neurodegenerative impairments.
Neuroprotective effect of peptides extracted from walnut (Juglans Sigilata Dode) proteins on Aβ25-35-induced memory impairment in mice
TLDR
Walnut peptide supplementation effectively ameliorated the cognitive deficits and memory impairment of mice and suggested that walnut peptides may have a protective effect on AD by reducing inflammatory responses and modulating antioxidant system.
Neuroprotective effect of peptides extracted from walnut (Juglans Sigilata Dode) proteins on Aβ25-35-induced memory impairment in mice
  • J. Zou, Pei-shan Cai, C. Xiong, J. Ruan
  • Biology
    Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • 2016
TLDR
Walnut peptide supplementation effectively ameliorated the cognitive deficits and memory impairment of mice and suggested that walnut peptides may have a protective effect on AD by reducing inflammatory responses and modulating antioxidant system.
Proline Rich Peptides of Neurohypophysial Origin: Related Peptides and Possible Functions
TLDR
Using the AutoDock vina software it was shown, that PRP-1 and its homologues strongly interact with receptors, such as: mouse phosphorylated mitogen activated protein kinase 14, mouse toll like receptor 4, human Ca-sensing receptor, human epithelial growth factor receptor and human superoxide dismutase 1.
The cerebrovascular effects of PRP-1
TLDR
The experimental results demonstrated the ability of PRP-1 to repair damaged cerebral blood flow caused by common carotid artery occlusion and the protein isolated is able to dilate the blood vessels of both the heart and the brain.
Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer’s Disease Model Rats by Maintaining Synaptic Plasticity
TLDR
It is shown that OA could ameliorate Aβ-induced memory loss of AD rats by maintaining synaptic plasticity of the hippocampus and TEM results showed OAcould alleviate neuron damage and synapses changes induced by Aβ25-35.
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References

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TLDR
There is evidence that PRP can differentially reduce both staurosporine- and doxorubicin-induced hippocampal and bone marrow cell apoptosis and protective effect of PRP-1 against apoptotic cell death was shown to be both time- and dose-dependent.
Preclinical Evidence of Neuroprotection by Cholinesterase Inhibitors
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Results show that cholinesterase inhibitors such as donepezil protect cortical neurons against glutamate neurotoxicity via α4β2 and α7 nicotinic acetylcholine receptors at least partly by inhibiting the process of apoptosis.
PRP-1 Protective Effect against Central and Peripheral Neurodegeneration following n. ischiadicus Transection
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It may be concluded that PRP-1 promotes nerve regeneration and may be used clinically to improve the outcome of peripheral nerve primary repair.
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TLDR
It was revealed considerably more expressed PRP action on neurodegenerative process connected to spinal cord injury (in comparison with DEX) and the influence of hormones was compared in identical conditions of experiments on non-injured (control) and injured sides.
Neuroprotective Action of Hypothalamic Peptide PRP-1 at Various Time Survivals Following Spinal Cord Hemisection
TLDR
PRP-1 administration, both daily and every other day, for a period of 2–3 weeks led to prevention of scar formation and promotion of the re-growth of white matter nerve fibers in the damaged area, and resulted in prevention of neuroglial elements degeneration and reduction in gliosis expression in the lesion supporting neuronal survival.
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TLDR
Based on the findings regarding PRP action on neurons survival, axons regeneration, and the number of IphF-Ir lymphocytes and NPY-Ir nerve fibers, PRP is suggested to act as a neuroprotector, functioning as a putative neurotransmitter and immunomodulator.
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