Abstract Details

Title Procognitive and neuroprotective effect of 5-HT7 agonist in an animal model by ICV amyloid-b injection

Topic Aging, Dementia, and Behavioral Neurology

Presentation(s) P1 - Poster Session 1 (5:30 PM-6:30 PM)

Poster/Presentation
Number 9-005

Objective The aim of this protocol was to investigate the role of LP-211, specific agonist of 5-HT7, on social recognition behavior and spatial memory and its possible neuroprotector effect in a neurodegeneration animal model.

Background The serotoninergic receptor 5-HT7 is a G-coupled receptor broadly expressed in the CNS. Its activation stimulates multiple downstream signaling cascades, including ERK, Akt and protein kinase B pathways which have been associated with neuroprotective features, as well as cdc-42 and other Rho-GTPases which stimulate neurite outgrowing by the activation of the cyclin-dependent protein kinase 5. The effects of β-A plaques on neuronal degeneration and on disruption of the serotoninergic system have been thoroughly studied, as well as different substances that may reverse this damage. However, the role of 5HT7 in a neurodegeneration model is yet to be determined.

Design/Methods Male adult Wistar rats, received an intracerebroventricular injection of different substances: saline solution (control groups), β-A1-42 , dimethyl sulfoxide or LP-211 and tested for social recognition behavior and spatial memory. Fluorojade technique was used to quantify degenerated neurons and thus analyze the neuroprotector effect of LP-211.

Results

The rats that were exposed to LP-211 + β-A1-42 showed a similar performance as the control rats. This performance was statistically significant in the social recognition memory test, as well as in the spontaneous alternation behaviour in a T-maze when compared to the group exposed only to the β-A 1-42. When analyzing the Fluoro-jade stainings the LP-211 + β-A 1-42 group showed statistically significant less degeneration compared to the β-A1-42 group.

Conclusions The agonism of 5-HT7 counteracts the nocive effect of β-A1-42 in the central nervous system, evidenced by the improvement in memory and in neuronal degeneration of the β-A-1-42 + LP211 group. This investigation could potentially lead to additional research that looks for new possible therapeutic options against neurodegenerative diseases.

Authors/Disclosures
Alejandro Quintero Villegas PRESENTER	No disclosure on file
	No disclosure on file
Maria Oa Valenzuela Almada	No disclosure on file
	No disclosure on file
	No disclosure on file

��ɫ��

��ɫ��