PMID- 37508898
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230731
IS  - 2306-5354 (Print)
IS  - 2306-5354 (Electronic)
IS  - 2306-5354 (Linking)
VI  - 10
IP  - 7
DP  - 2023 Jul 23
TI  - Cognitive Impairment in Multiple Sclerosis.
LID - 10.3390/bioengineering10070871 [doi]
LID - 871
AB  - Almost three million individuals suffer from multiple sclerosis (MS) throughout 
      the world, a demyelinating disease in the nervous system with increased 
      prevalence over the last five decades, and is now being recognized as one 
      significant etiology of cognitive loss and dementia. Presently, disease modifying 
      therapies can limit the rate of relapse and potentially reduce brain volume loss 
      in patients with MS, but unfortunately cannot prevent disease progression or the 
      onset of cognitive disability. Innovative strategies are therefore required to 
      address areas of inflammation, immune cell activation, and cell survival that 
      involve novel pathways of programmed cell death, mammalian forkhead transcription 
      factors (FoxOs), the mechanistic target of rapamycin (mTOR), AMP activated 
      protein kinase (AMPK), the silent mating type information regulation 2 homolog 1 
      (Saccharomyces cerevisiae) (SIRT1), and associated pathways with the 
      apolipoprotein E (APOE-epsilon4) gene and severe acute respiratory syndrome coronavirus 
      (SARS-CoV-2). These pathways are intertwined at multiple levels and can involve 
      metabolic oversight with cellular metabolism dependent upon nicotinamide adenine 
      dinucleotide (NAD+). Insight into the mechanisms of these pathways can provide 
      new avenues of discovery for the therapeutic treatment of dementia and loss in 
      cognition that occurs during MS.
FAU - Maiese, Kenneth
AU  - Maiese K
AUID- ORCID: 0000-0002-5049-9116
AD  - Cellular and Molecular Signaling, New York, NY 10022, USA.
LA  - eng
GR  - NS053956/NH/NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20230723
PL  - Switzerland
TA  - Bioengineering (Basel)
JT  - Bioengineering (Basel, Switzerland)
JID - 101676056
PMC - PMC10376413
OTO - NOTNLM
OT  - APOE-epsilon4
OT  - COVID-19
OT  - FoxO
OT  - SIRT1
OT  - apoptosis
OT  - autophagy
OT  - dementia
OT  - mTOR
OT  - multiple sclerosis
OT  - nicotinamide
COIS- The author declares no conflict of interest.
EDAT- 2023/07/29 11:53
MHDA- 2023/07/29 11:54
PMCR- 2023/07/23
CRDT- 2023/07/29 01:09
PHST- 2023/06/20 00:00 [received]
PHST- 2023/07/19 00:00 [revised]
PHST- 2023/07/21 00:00 [accepted]
PHST- 2023/07/29 11:54 [medline]
PHST- 2023/07/29 11:53 [pubmed]
PHST- 2023/07/29 01:09 [entrez]
PHST- 2023/07/23 00:00 [pmc-release]
AID - bioengineering10070871 [pii]
AID - bioengineering-10-00871 [pii]
AID - 10.3390/bioengineering10070871 [doi]
PST - epublish
SO  - Bioengineering (Basel). 2023 Jul 23;10(7):871. doi: 
      10.3390/bioengineering10070871.