The Energy Metabolism Dysfunction in Psychiatric Disorders Postmortem Brains: Focus on Proteomic Evidence
“Given the importance of energy metabolism in the brain and its important role in the pathophysiology of neuropsychiatric disorders, this review aims to compile data on energy metabolism dysfunction found on postmortem brain tissue revealed by proteomics in SCZ, BPD, and MDD.”
I don’t really comprehend a lot of this article except the connection to energy metabolism dysfunction. To those who have greater understanding of the terminology, do you find anything significant/relevant in this article? Ray Peat has said that paranoia and hallucinations are a result of low brain metabolism and inflammation. I am looking for information that supports his view and thought this article might do that. @haidut If you have time, could you read this review and post your opinion?
“The antipsychotic drug clozapine was reported to elevate the erythrocyte levels of AA and docosahexaenoic acid (DHA) in SCZ patients (Glen et al., 1996). This could indicate an additional mechanism that contributes to the therapeutic effects of clozapine (Horrobin, 1998)”
“Given the importance of energy metabolism in the brain and its important role in the pathophysiology of neuropsychiatric disorders, this review aims to compile data on energy metabolism dysfunction found on postmortem brain tissue revealed by proteomics in SCZ, BPD, and MDD.”
I don’t really comprehend a lot of this article except the connection to energy metabolism dysfunction. To those who have greater understanding of the terminology, do you find anything significant/relevant in this article? Ray Peat has said that paranoia and hallucinations are a result of low brain metabolism and inflammation. I am looking for information that supports his view and thought this article might do that. @haidut If you have time, could you read this review and post your opinion?
“The antipsychotic drug clozapine was reported to elevate the erythrocyte levels of AA and docosahexaenoic acid (DHA) in SCZ patients (Glen et al., 1996). This could indicate an additional mechanism that contributes to the therapeutic effects of clozapine (Horrobin, 1998)”
