PMID- 33920212
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210518
IS  - 2227-9059 (Print)
IS  - 2227-9059 (Electronic)
IS  - 2227-9059 (Linking)
VI  - 9
IP  - 4
DP  - 2021 Apr 10
TI  - Nicotinamide Ameliorates Amyloid Beta-Induced Oxidative Stress-Mediated 
      Neuroinflammation and Neurodegeneration in Adult Mouse Brain.
LID - 10.3390/biomedicines9040408 [doi]
LID - 408
AB  - Alzheimer's disease (AD) is the most predominant age-related neurodegenerative 
      disease, pathologically characterized by the accumulation of aggregates of 
      amyloid beta Abeta(1-42) and tau hyperphosphorylation in the brain. It is considered 
      to be the primary cause of cognitive dysfunction. The aggregation of Abeta(1-42) 
      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 Abeta(1-42) -induced neurotoxicity was 
      investigated in mouse brains. Intracerebroventricular (i.c.v.) Abeta(1-42) injection 
      elicited neuronal dysfunctions that led to memory impairment and 
      neurodegeneration in mouse brains. After 24 h after Abeta(1-42) 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 Abeta(1-42)-injected mouse brains, where the 
      regulation of p-JNK further regulated inflammatory marker proteins (TNF-alpha, IL-1beta, 
      transcription factor NF-kB) and apoptotic marker proteins (Bax, caspase 3, 
      PARP1). Furthermore, NAM + Abeta 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 Abeta(1-42) -induced memory deficits. Collectively, the results of 
      this study suggest that NAM may be a potential preventive and therapeutic 
      candidate for Abeta(1-42) -induced reactive oxygen species (ROS)-mediated 
      neuroinflammation, neurodegeneration, and neurotoxicity in an adult mouse model.
FAU - Rehman, Inayat Ur
AU  - Rehman IU
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
FAU - Ahmad, Riaz
AU  - Ahmad R
AUID- ORCID: 0000-0001-7411-9483
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
FAU - Khan, Ibrahim
AU  - Khan I
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
FAU - Lee, Hyeon Jin
AU  - Lee HJ
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
FAU - Park, Jungsung
AU  - Park J
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
FAU - Ullah, Rahat
AU  - Ullah R
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
FAU - Choi, Myeong Jun
AU  - Choi MJ
AD  - Research and Development Center, Axceso Bio-pharma co, Anyang 14056, Korea.
FAU - Kang, Hee Young
AU  - Kang HY
AD  - Department of Neurology, Gyeongsang National University Hospital, Gyeongsang 
      National University College of Medicine, Jinju 52828, Korea.
FAU - Kim, Myeong Ok
AU  - Kim MO
AD  - Division of Life Sciences and Applied Life Science (BK 21 Four), College of 
      Natural Science, Gyeongsang National University, Jinju 52828, Korea.
LA  - eng
PT  - Journal Article
DEP - 20210410
PL  - Switzerland
TA  - Biomedicines
JT  - Biomedicines
JID - 101691304
PMC - PMC8070416
OTO - NOTNLM
OT  - ROS
OT  - neurodegeneration
OT  - neuroinflammation
OT  - nicotinamide
OT  - oxidative stress
COIS- All authors declare no conflict of interest.
EDAT- 2021/05/01 06:00
MHDA- 2021/05/01 06:01
PMCR- 2021/04/10
CRDT- 2021/04/30 01:14
PHST- 2021/02/23 00:00 [received]
PHST- 2021/03/22 00:00 [revised]
PHST- 2021/04/06 00:00 [accepted]
PHST- 2021/04/30 01:14 [entrez]
PHST- 2021/05/01 06:00 [pubmed]
PHST- 2021/05/01 06:01 [medline]
PHST- 2021/04/10 00:00 [pmc-release]
AID - biomedicines9040408 [pii]
AID - biomedicines-09-00408 [pii]
AID - 10.3390/biomedicines9040408 [doi]
PST - epublish
SO  - Biomedicines. 2021 Apr 10;9(4):408. doi: 10.3390/biomedicines9040408.