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

Abstract

Systemic administration of PRP-1 possesses neuroprotective effects and can prevent the neurodegeneration in hippocampus induced by Abeta25-35. This suggests that PRP-1 could be a potential therapeutic agent for specific neurodegenerative diseases.

Disruption of Cholinergic Circuits as an Area for Targeted Drug Treatment of Alzheimer’s Disease: In Vivo Assessment of Short-Term Plasticity in Rat Brain

“…Moreover, our previous studies revealed a deficit of working and spatial memory in rats following modeling of AD by intracerebroventricular (i.c.v.) injection of Aβ 25–35, at later dates (60th, 90th days and more after Aβ 25–35 administration) [ 28 , 30 , 31 ].…”

Morphofunctional Correlation of Excitatory and Depressor Synaptic Processes in Hippocampus, Amygdala and Basal Meynert Nucleus Neurons in Dynamics of Development of Alzheimer's Disease Model Induced by Aβ25-35

“…In confirmation, the modern studies on the cellular and network levels show that synaptic inhibition cannot be assessed only as opposed to synaptic excitation and additionally serves highly specific functions in the nervous system of mammals [71]. Moreover, sustainable deepening of depression in our above-mentioned works is the result of involvement as a protective categories Galarmin or PRP-1 (proine-rich peptide), the hypothalamic neuropeptide-immunomodulator, snake venoms, parathyroid hormone (PTH), and others [50,62,63,72,73] and adrenalectomy [74][75][76] on the activity of H neurons in the amyloid model оf AD.…”

“…According to our own data, depressor response more intensively involved of both in the nonspecific (peripheral and central) and specific neurodegeneration [50][51][52]. It is supposed the advancement deepening the tetanic depression as assisting the recovery of the initial ratio of excitatory and depressor responses.…”

“…It is shown that depressor post-stimulus manifestations in the form TD and PTD mediate GABA or glycine monoamines. Us shows the protective purpose of GABA in studies of nonspecific neurodegeneration, especially in the Deiters' nucleus (following unilateral labyrinthectomy) [51], in the spinal cord after lateral hemisection [53][54][55][56] on peripheral nerve injury [57][58][59][60][61], on amyloid model of AD [50,62,63] and also on the rotenone model of PD [64,65]; in neurons mainly the GABAergic nature, in which early involving depressor reactions are accompanied by the recovery process until its completion. Confirmation the assumption of the universal protective assignment of GABA-ergic inhibition is the fact that in some systems during development of the nervous system GABA promotes proliferation, migration, differentiation and maturation of the synapse, expression of the GABA(A) receptor [66].…”

Protective Effects of Hypothalamic Proline-Rich Peptide and Cobra Venom Naja Naja Oxiana on Dynamics of Vestibular Compensation Following Unilateral Labyrinthectomy

“…Most study represents PRP-1, which has large spectrum of biological action on immune and nervous system, as well as universal protective effect on neurodegenerative processes [11,12]. Earlier was shown the protective effect of PRP-1 during peripheral and central neurodegeneration [13][14][15][16][17][18][19][20][21][22].…”