Nicotinamide Ameliorates Amyloid Beta-Induced Oxidative Stress-Mediated Neuroinflammation and Neurodegeneration in Adult Mouse Brain

WHOM is going to put two and two together and create research on nicotinamide in humans? This earlier one on TBI and this one on mouse brains should trigger research on stroke. At least it would if there were two functioning neurons anywhere in stroke leadership. 

A COMBINATION THERAPY OF NICOTINAMIDE AND PROGESTERONE FOR FUNCTIONAL RECOVERY FOLLOWING TRAUMATIC BRAIN INJURY

 July 2013

 

The latest here:

 Nicotinamide Ameliorates Amyloid Beta-Induced OxidativeStress-Mediated Neuroinflammation and Neurodegeneration inAdult Mouse Brain

Inayat Ur Rehman 1 , 

Riaz Ahmad 1 , 

Ibrahim Khan 1 , 

Hyeon Jin Lee 1 , 

Jungsung Park 1 , 

Rahat Ullah 1 , 

Myeong Jun Choi 2 , 

Hee Young Kang 3 

Myeong Ok Kim 1,*


 Citation: Rehman, I.U.; Ahmad, R.; Khan, I.; Lee, H.J.; Park, J.; Ullah, R.; Choi, M.J.; Kang, H.Y.; Kim, M.O. Nicotinamide Ameliorates Amyloid Beta-Induced Oxidative Stress-Mediated Neuroinflammation and Neurodegeneration in Adult Mouse Brain. Biomedicines 2021, 9, 408. https://doi.org/10.3390/ biomedicines9040408 Academic Editor: Rosana Di Paola Received: 23 February 2021 Accepted: 6 April 2021 Published: 10 April 2021 Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). 

1 Division of Life Sciences and Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea; inayaturrehman201516@gnu.ac.kr (I.U.R.); riazk0499@gnu.ac.kr (R.A.); ibrahim1994@gnu.ac.kr (I.K.); lhj4912@gnu.ac.kr (H.J.L.); jsp@gnu.ac.kr (J.P.); rahatullah1414@gnu.ac.kr (R.U.) 

2 Research and Development Center, Axceso Bio-pharma co, Anyang 14056, Korea; myeongjun@gmail.com 3 Department of Neurology, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, Jinju 52828, Korea; miranda75@naver.com * Correspondence: mokim@gnu.ac.kr; Tel.: +82-55-772-1345; Fax: +82-55-772-2656 

Abstract: 

Alzheimer’s disease (AD) is the most predominant age-related neurodegenerative disease, pathologically characterized by the accumulation of aggregates of amyloid beta Aβ1–42 and tau hyperphosphorylation in the brain. It is considered to be the primary cause of cognitive dysfunction. The aggregation of Aβ1–42 leads to neuronal inflammation and apoptosis. Since vitamins are basic dietary nutrients that organisms need for their growth, survival, and other metabolic functions, in this study, the underlying neuroprotective mechanism of nicotinamide (NAM) Vitamin B3 against Aβ1–42 -induced neurotoxicity was investigated in mouse brains. Intracerebroventricular (i.c.v.) Aβ1–42 injection elicited neuronal dysfunctions that led to memory impairment and neurodegeneration in mouse brains. After 24 h after Aβ1–42 injection, the mice were treated with NAM (250 mg/kg intraperitoneally) for 1 week. For biochemical and Western blot studies, the mice were directly sacrificed, while for confocal and “immunohistochemical staining”, mice were perfused transcardially with 4% paraformaldehyde. Our biochemical, immunofluorescence, and immunohistochemical results showed that NAM can ameliorate neuronal inflammation and apoptosis by reducing oxidative stress through lowering malondialdehyde and 2,7-dichlorofluorescein levels in an Aβ1–42-injected mouse brains, where the regulation of p-JNK further regulated inflammatory marker proteins (TNF-α, IL-1β, transcription factor NF-kB) and apoptotic marker proteins (Bax, caspase 3, PARP1). Furthermore, NAM + Aβ treatment for 1 week increased the amount of survival neurons and reduced neuronal cell death in Nissl staining. We also analyzed memory dysfunction via behavioral studies and the analysis showed that NAM could prevent Aβ1–42 -induced memory deficits. Collectively, the results of this study suggest that NAM may be a potential preventive and therapeutic candidate for Aβ1–42 -induced reactive oxygen species (ROS)-mediated neuroinflammation, neurodegeneration, and neurotoxicity in an adult mouse model.