PMID- 38365306
OWN - NLM
STAT- MEDLINE
DCOM- 20240226
LR  - 20240226
IS  - 1469-5111 (Electronic)
IS  - 1461-1457 (Print)
IS  - 1461-1457 (Linking)
VI  - 27
IP  - 2
DP  - 2024 Feb 1
TI  - PI3K-AKT/mTOR Signaling in Psychiatric Disorders: A Valuable Target to Stimulate 
      or Suppress?
LID - 10.1093/ijnp/pyae010 [doi]
LID - pyae010
AB  - Economic development and increased stress have considerably increased the 
      prevalence of psychiatric disorders in recent years, which rank as some of the 
      most prevalent diseases globally. Several factors, including chronic social 
      stress, genetic inheritance, and autogenous diseases, lead to the development and 
      progression of psychiatric disorders. Clinical treatments for psychiatric 
      disorders include psychotherapy, chemotherapy, and electric shock therapy. 
      Although various achievements have been made researching psychiatric disorders, 
      the pathogenesis of these diseases has not been fully understood yet, and serious 
      adverse effects and resistance to antipsychotics are major obstacles to treating 
      patients with psychiatric disorders. Recent studies have shown that the mammalian 
      target of rapamycin (mTOR) is a central signaling hub that functions in nerve 
      growth, synapse formation, and plasticity. The PI3K-AKT/mTOR pathway is a 
      critical target for mediating the rapid antidepressant effects of these 
      pharmacological agents in clinical and preclinical research. Abnormal 
      PI3K-AKT/mTOR signaling is closely associated with the pathogenesis of several 
      neurodevelopmental disorders. In this review, we focused on the role of mTOR 
      signaling and the related aberrant neurogenesis in psychiatric disorders. 
      Elucidating the neurobiology of the PI3K-AKT/mTOR signaling pathway in 
      psychiatric disorders and its actions in response to antidepressants will help us 
      better understand brain development and quickly identify new therapeutic targets 
      for the treatment of these mental illnesses.
CI  - (c) The Author(s) 2024. Published by Oxford University Press on behalf of CINP.
FAU - Chen, Yan
AU  - Chen Y
AD  - Department of Neurology, Nantong Third People's Hospital, Affiliated Nantong 
      Hospital 3 of Nantong University, Nantong, Jiangsu, China.
FAU - Guan, Wei
AU  - Guan W
AD  - Department of Pharmacology, Pharmacy College, Nantong University, Nantong, 
      Jiangsu, China.
FAU - Wang, Mei-Lan
AU  - Wang ML
AD  - Department of Neurology, Nantong Third People's Hospital, Affiliated Nantong 
      Hospital 3 of Nantong University, Nantong, Jiangsu, China.
FAU - Lin, Xiao-Yun
AU  - Lin XY
AD  - Department of Neurology, Nantong Third People's Hospital, Affiliated Nantong 
      Hospital 3 of Nantong University, Nantong, Jiangsu, China.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Int J Neuropsychopharmacol
JT  - The international journal of neuropsychopharmacology
JID - 9815893
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - W36ZG6FT64 (Sirolimus)
RN  - 0 (Antidepressive Agents)
SB  - IM
MH  - Humans
MH  - *Proto-Oncogene Proteins c-akt/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Sirolimus/pharmacology
MH  - Antidepressive Agents/pharmacology
MH  - *Mental Disorders/drug therapy
PMC - PMC10888523
OTO - NOTNLM
OT  - Depression
OT  - PI3K-AKT
OT  - Psychiatric disorders
OT  - Signaling pathway
OT  - Targets
OT  - mTOR
EDAT- 2024/02/17 10:42
MHDA- 2024/02/26 06:43
PMCR- 2024/02/14
CRDT- 2024/02/16 20:52
PHST- 2023/09/22 00:00 [received]
PHST- 2024/02/08 00:00 [accepted]
PHST- 2024/02/26 06:43 [medline]
PHST- 2024/02/17 10:42 [pubmed]
PHST- 2024/02/16 20:52 [entrez]
PHST- 2024/02/14 00:00 [pmc-release]
AID - 7608050 [pii]
AID - pyae010 [pii]
AID - 10.1093/ijnp/pyae010 [doi]
PST - ppublish
SO  - Int J Neuropsychopharmacol. 2024 Feb 1;27(2):pyae010. doi: 10.1093/ijnp/pyae010.