scholarly journals Altered Expression of Endoplasmic Reticulum Stress-Related Genes in the Middle Frontal Cortex of Subjects with Autism Spectrum Disorder

2017 ◽  
Vol 3 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Amanda Crider ◽  
Anthony O. Ahmed ◽  
Anilkumar Pillai
2020 ◽  
Vol 14 (2) ◽  
pp. 170-174
Author(s):  
Koichi Kawada ◽  
Nobuyuki Kuramoto ◽  
Seisuke Mimori

: Autism spectrum disorder (ASD) is a neurodevelopmental disease, and the number of patients has increased rapidly in recent years. The causes of ASD involve both genetic and environmental factors, but the details of causation have not yet been fully elucidated. Many reports have investigated genetic factors related to synapse formation, and alcohol and tobacco have been reported as environmental factors. This review focuses on endoplasmic reticulum stress and amino acid cycle abnormalities (particularly glutamine and glutamate) induced by many environmental factors. In the ASD model, since endoplasmic reticulum stress is high in the brain from before birth, it is clear that endoplasmic reticulum stress is involved in the development of ASD. On the other hand, one report states that excessive excitation of neurons is caused by the onset of ASD. The glutamine-glutamate cycle is performed between neurons and glial cells and controls the concentration of glutamate and GABA in the brain. These neurotransmitters are also known to control synapse formation and are important in constructing neural circuits. Theanine is a derivative of glutamine and a natural component of green tea. Theanine inhibits glutamine uptake in the glutamine-glutamate cycle via slc38a1 without affecting glutamate; therefore, we believe that theanine may prevent the onset of ASD by changing the balance of glutamine and glutamate in the brain.


Author(s):  
Kasra Honarmand Tamizkar ◽  
Soudeh Ghafouri-Fard ◽  
Mir Davood Omrani ◽  
Farkhondeh Pouresmaeili ◽  
Shahram Arsang-Jang ◽  
...  

2015 ◽  
Vol 126 (8) ◽  
pp. e91-e92 ◽  
Author(s):  
E. Hoffmann ◽  
C. Brück ◽  
B. Kreifelts ◽  
T. Ethofer ◽  
D. Wildgruber

2016 ◽  
Vol 123 (8) ◽  
pp. 937-947 ◽  
Author(s):  
Elgin Hoffmann ◽  
Carolin Brück ◽  
Benjamin Kreifelts ◽  
Thomas Ethofer ◽  
Dirk Wildgruber

Gene Reports ◽  
2021 ◽  
pp. 101172
Author(s):  
Mohammad Taheri ◽  
Zahra Younesi ◽  
Sahar Moradi ◽  
Kasra Honarmand Tamizkar ◽  
Katayoon Razjouyan ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1346
Author(s):  
Marco Colizzi ◽  
Riccardo Bortoletto ◽  
Rosalia Costa ◽  
Leonardo Zoccante

Autism spectrum disorder (ASD) pathophysiology is not completely understood; however, altered inflammatory response and glutamate signaling have been reported, leading to the investigation of molecules targeting the immune-glutamatergic system in ASD treatment. Palmitoylethanolamide (PEA) is a naturally occurring saturated N-acylethanolamine that has proven to be effective in controlling inflammation, depression, epilepsy, and pain, possibly through a neuroprotective role against glutamate toxicity. Here, we systematically reviewed all human and animal studies examining PEA and its biobehavioral correlates in ASD. Studies indicate altered serum/brain levels of PEA and other endocannabinoids (ECBs)/acylethanolamines (AEs) in ASD. Altered PEA signaling response to social exposure and altered expression/activity of enzymes responsible for the synthesis and catalysis of ECBs/AEs, as well as downregulation of the peroxisome proliferator activated receptor-α (PPAR-α) and cannabinoid receptor target GPR55 mRNA brain expression, have been reported. Stress and exposure to exogenous cannabinoids may modulate ECBs/AEs levels and expression of candidate genes for neuropsychiatric disorders, with implications for ASD. Limited research suggests that PEA supplementation reduces overall autism severity by improving language and social and nonsocial behaviors. Potential neurobiological underpinnings include modulation of immune response, neuroinflammation, neurotrophy, apoptosis, neurogenesis, neuroplasticity, neurodegeneration, mitochondrial function, and microbiota activity, possibly through peroxisome proliferator-activated receptor-α (PPAR-α) activation.


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