Action of the hypothalamic proline-rich peptide and cobra venom during vestibular compensation following unilateral labyrinthectomy

Alzheimer disease (AD) is the most common form of dementia in the elderly that
slowly destroys memory and cognitive functions. The disease has no cure and leads to significant
structural and functional brain abnormalities. To facilitate the treatment of this disease, we aimed
to investigate proline-rich peptide (PRP-1) action of hypothalamus on hippocampal (HP) neurons
and dynamics of their recovery, after intracerebroventricular (ICV) injection of amyloid-β (Aβ).
Methods: Experiments were carried out on 24 adult, male Albino rats (average weight: 230±30
g). The animals were randomly divided into 3 groups (control, Aβ, and Aβ plus PRP-1).
Electrophysiological patterns of hippocampal neurons in response to stimulation of entorhinal
cortex (EC) with high frequency stimulation (50 Hz) were studied.
Results: It was found that Aβ (25-35) suppresses the electrical activity of hippocampal neurons.
The PRP-1 would return this activity to normal levels.
Conclusion: In general, PRP-1 has protective effect against AD-related alterations induced by
amyloid peptides. This protective effect is probably due to stimulation of the immune and glia
system