PMID- 38277116
OWN - NLM
STAT- MEDLINE
DCOM- 20240715
LR  - 20240715
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 61
IP  - 8
DP  - 2024 Aug
TI  - Prenatal Programming of Monocyte Chemotactic Protein-1 Signaling in Autism 
      Susceptibility.
PG  - 6119-6134
LID - 10.1007/s12035-024-03940-z [doi]
AB  - Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder that 
      involves functional and structural defects in selective central nervous system 
      (CNS) regions, harming the individual capability to process and respond to 
      external stimuli, including impaired verbal and non-verbal communications. 
      Etiological causes of ASD have not been fully clarified; however, prenatal 
      activation of the innate immune system by external stimuli might infiltrate 
      peripheral immune cells into the fetal CNS and activate cytokine secretion by 
      microglia and astrocytes. For instance, genomic and postmortem histological 
      analysis has identified proinflammatory gene signatures, microglia-related 
      expressed genes, and neuroinflammatory markers in the brain during ASD diagnosis. 
      Active neuroinflammation might also occur during the developmental stage, 
      promoting the establishment of a defective brain connectome and increasing 
      susceptibility to ASD after birth. While still under investigation, we tested the 
      hypothesis whether the monocyte chemoattractant protein-1 (MCP-1) signaling is 
      prenatally programmed to favor peripheral immune cell infiltration and activate 
      microglia into the fetal CNS, setting susceptibility to autism-like behavior. In 
      this review, we will comprehensively provide the current understanding of the 
      prenatal activation of MCP-1 signaling by external stimuli during the 
      developmental stage as a new selective node to promote neuroinflammation, brain 
      structural alterations, and behavioral defects associated to ASD diagnosis.
CI  - (c) 2024. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Camacho-Morales, Alberto
AU  - Camacho-Morales A
AUID- ORCID: 0000-0002-2588-9489
AD  - College of Medicine, Department of Biochemistry, Universidad Autonoma de Nuevo 
      Leon, Monterrey, NL, Mexico. acm590@hotmail.com.
AD  - Center for Research and Development in Health Sciences, Neurometabolism Unit, 
      Universidad Autonoma de Nuevo Leon, San Nicolas de los Garza, Monterrey, NL, 
      Mexico. acm590@hotmail.com.
FAU - Cardenas-Tueme, Marcela
AU  - Cardenas-Tueme M
AD  - Tecnologico de Monterrey, Escuela de Medicina y Ciencias de La Salud and The 
      Institute for Obesity Research, 64710, Monterrey, Mexico.
AD  - Nutrition Unit, Center for Research and Development in Health Sciences, 
      Universidad Autonoma de Nuevo Leon, 64460, Monterrey, Mexico.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20240126
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Humans
MH  - *Chemokine CCL2/metabolism
MH  - *Signal Transduction
MH  - Animals
MH  - Disease Susceptibility
MH  - Autistic Disorder/metabolism/pathology
MH  - Female
MH  - Microglia/metabolism/pathology
MH  - Pregnancy
MH  - Autism Spectrum Disorder/metabolism/pathology
MH  - Brain/metabolism/pathology
MH  - Fetal Development/physiology
OTO - NOTNLM
OT  - Autism
OT  - Chemokines
OT  - Microglia
OT  - Neuroinflammation
OT  - Prenatal programming
EDAT- 2024/01/26 12:43
MHDA- 2024/07/15 12:42
CRDT- 2024/01/26 11:09
PHST- 2023/09/12 00:00 [received]
PHST- 2024/01/11 00:00 [accepted]
PHST- 2024/07/15 12:42 [medline]
PHST- 2024/01/26 12:43 [pubmed]
PHST- 2024/01/26 11:09 [entrez]
AID - 10.1007/s12035-024-03940-z [pii]
AID - 10.1007/s12035-024-03940-z [doi]
PST - ppublish
SO  - Mol Neurobiol. 2024 Aug;61(8):6119-6134. doi: 10.1007/s12035-024-03940-z. Epub 
      2024 Jan 26.