Dover M, Moseley T, Biskaduros A, Paulchakrabarti M, Hwang SH, Hammock B, Choudhury B, Kaczor-Urbanowicz KE, Urbanowicz A, Morselli M, Dang J, Pellegrini M, Paul K, Bentolila LA, Fiala M. Polyunsaturated Fatty Acids Mend Macrophage Transcriptome, Glycome, and Phenotype in the Patients with Neurodegenerative Diseases, Including Alzheimer's Disease. J Alzheimers Dis. 2023;91(1):245-261. PubMed.
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UCLA
I would like to submit a comment on our paper:
We performed a study of Alzheimer’s disease and other neurodegenerative patients’ monocyte/macrophages. Monocytes circulate in the blood, migrate into the brain, and clear Aβ in healthy people, but are defective in AD patients. Our study demonstrates that molecular defects in the transcriptome and glycome of macrophages cause faulty clearance of Aβ brain deposits. The study explains that defects in glycolysis and oxidative phosphorylation make macrophages defective in energy and glycosylation, and lead to flawed uptake and degradation of Aβ in plaques. Although AD macrophages upload some Aβ they are unable to degrade it, and they release it into “congophilic” vessels with cerebro-vascular amyloid angiopathy. Thus, the molecular defects of AD patients are a double whammy for the brain: lack of Aβ clearance and degradation.
On the positive side, we show that polyunsaturated fatty acids (PUFA) repair defects in the transcriptome and glycome of AD macrophages and mend their phenotype for uptake and degradation of Aβ. The repair by PUFA of the molecular defects and functions in Aβ uptake and degradation is incomplete and, in this study, was restricted to eight early subjective and mild cognitive impairment (MCI) patients. In a previous study, PUFA supplementation delayed the progression of MCI to dementia by four years.
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