Premium
[P3–149]: HSV‐1‐SPECIFIC IGG3 TITERS AND NEUTRALIZING ACTIVITY ARE REDUCED IN AD PATIENTS
Author(s) -
Agostini Simone,
Mancuso Roberta,
Calabrese Elena,
Hernis Ambra,
Nemni Raffaello,
Clerici Mario
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.06.1360
Subject(s) - neutralizing antibody , titer , herpes simplex virus , antibody , immunoglobulin g , virology , immunology , neutralization , immune system , medicine , virus
hypothesis and tau hypothesis. When it comes to aging, telomere length is thought to play important roles. In the present study, we compared telomere length between AD models and normal and evaluated the effects of a novel peptide mimicking telomerase on telomere length and disease progression in AD models. Methods:To evaluate the alteration of telomere length, neural stem cells (NSCs) were treated with oligomeric forms of amyloid b (Ab) and AD model mice were compared with wild type mice. A novel peptide with 16 amino acids of hTERT and it was treated to NSCs injured by Ab once and AD model mice three times a week for up to 4 months. Most of all, telomere length was compared depending on their conditions. In case of NSCs, the alterations of stem cell characteristics, including proliferation, migration, and so on, were evaluated after the treatment with Ab and the peptide. For AD model mice, neurobehavioral functions such as passive avoidance test and Y maze test were compared between control and treatment groups. After then, diverse molecular works, including western blotting, immunohistochemistry, etc., were done to measure the effect of the novel peptide on the pathogenic mechanisms of AD model mouse. Results: The telomere length of NSCs and AD model mice’s brains was significantly decreased by amyloid beta and aging, respectively. However, the novel peptide markedly increased it. In addition, the treatment of the peptide restored the characteristics of NSCs injured by Ab and improved neurobehavioral functions of AD model mice. All these beneficial effects looked associated with good effects of telomerase including extra-telomeric functions. Conclusions: In conclusion, we might need to look into other pathogenic mechanisms of AD when considering that therapeutic strategies based on amyloid hypothesis have not yet been successful and pathologic aging might be one of them. If then, the way to increase telomere length could be an alternative option for the treatment of AD.