Nicotinamide Reduces Amyloid Precursor Protein and Presenilin 1 in Brain Tissues of Amyloid Beta-Tail Vein Injected Mice.
- Author:
Eun Jin KIM
1
;
Soo Jin YANG
Author Information
- Publication Type:research-article
- Keywords: Aging; Alzheimer disease; β-amyloid; Niacin
- MeSH: Acclimatization; Aging; Alzheimer Disease; Amyloid*; Animals; Blotting, Western; Brain*; Gene Expression; Humans; Male; Mice*; NF-kappa B; Niacin; Niacinamide*; Presenilin-1*; Presenilins*; Sirtuin 1; Tail; Veins*
- From:Clinical Nutrition Research 2017;6(2):130-135
- CountryRepublic of Korea
- Language:English
- Abstract: The purpose of this study is to investigate whether nicotinic acid (NA) and nicotinamide (NAM) reduce the Alzheimer disease (AD)-related gene expression in brain tissues of amyloid beta (Aβ)-injected mice. Male Crj:CD1 (ICR) mice were divided into 6 treatment groups; 1) control, 2) Aβ control, 3) Aβ + NA 20 mg/kg/day (NA20), 4) Aβ + NA40, 5) Aβ + NAM 200 mg/kg/day (NAM200), and 6) Aβ + NAM400. After 1-week acclimation period, the mice orally received NA or NAM once a day for a total of 7 successive days. On day 7, biotinylated Aβ42 was injected into mouse tail vein. At 5 hours after the injection, blood and tissues were collected. Aβ42 injection was confirmed by Western blot analysis of Aβ42 protein in brain tissue. NAM400 pre-treatment significantly reduced the gene expression of amyloid precursor protein and presenilin 1 in brain tissues. And, NAM200 and NAM400 pre-treatments significantly increased sirtuin 1 expression in brain tissues, which is accompanied by the decreased brain expression of nuclear factor kappa B by 2 doses of NAM. Increased expression of AD-related genes was attenuated by the NAM treatment, which suggests that NAM supplementation may be a potential preventive strategy against AD-related deleterious changes.
