A medicine and food homology formula prevents cognitive deficits by inhibiting neuroinflammation and oxidative stress via activating AEA–Trpv1–Nrf2 pathway DOI
Mingjie Li, Jingyi Xu,

Hua-Yue Zhang

et al.

Inflammopharmacology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 21, 2024

Language: Английский

The Impact of High-Dose Fish Oil Supplementation on Mfsd2a, Aqp4, and Amyloid-β Expression in Retinal Blood Vessels of 5xFAD Alzheimer’s Mouse Model DOI Open Access
Irena Jovanović Macura, Desanka Milanović, Vesna Tešić

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(17), P. 9400 - 9400

Published: Aug. 29, 2024

In patients with Alzheimer’s disease (AD) and in animal models, the increased accumulation of amyloid β (Aβ) retinal blood vessels strongly correlates brain deposits cognitive decline. The Aβ may result from impaired transcytosis a dysfunctional ocular glymphatic system AD. High-dose fish oil (FO) supplementation has been shown to significantly change expression major facilitator superfamily domain-containing protein 2a (Mfsd2a), key regulator transcytosis, Aquaporin 4 (Aqp4), an essential component retinas WT mice. We examined Mfsd2a Aqp4 4-month-old 5xFAD female mice supplemented high-dose FO for three weeks. There was significant increase compared control Additionally, observed retinas, indicative system, decreased. Simultaneously, reduced following supplementation. These findings suggest that could serve as adjunct developing new treatments aimed at improving regulation or function AD retina.

Language: Английский

Citations

1

The cerebral blood flow response to neuroactivation is reduced in cognitively normal men with β-amyloid accumulation DOI Creative Commons
Mark Bitsch Vestergaard, Aftab Bakhtiari, Merete Osler

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: March 29, 2024

Abstract Background Accumulation of β-amyloid (Aβ) in the brain is a hallmark Alzheimer’s Disease (AD). Cerebral deposition Aβ initiates deteriorating pathways which eventually can lead to AD. However, exact mechanisms are not known. A possible pathway could be that affects cerebral vessels, causing inadequate cerebrovascular function. In present study, we examined if accumulation associated with reduced blood flow response (CBF) neuronal activation by visual stimulation (DCBFVis.Act) cognitively normal subjects from Metropolit Danish Male Birth Cohort. Methods 64 participated study. DCBFVis.Act was measured using arterial spin labelling (ASL) combined blood-oxygen-level-dependent (BOLD) MRI. Neuronal obtained flickering checkerboard presented on screen MRI-scanner. Brain and glucose metabolism were assessed PET imaging radiotracers [11C]Pittsburgh Compound-B (PiB) [18F]Fluorodeoxyglucose (FDG), respectively. Cortical thickness structural Results correlated negatively (\(\beta\) = -32.1 [95% confidence interval (CI): -60.2 ; -4.1], r -0.30, p 0.025) PiB standardized uptake value ratio (SUVr) regions activated stimulation. did correlate FDG SUVr 1.9 [CI: -23.8 27.6], 0.02, 0.88) or cortical 10.3 -8.4 29.0], 0.15, 0.27) regions. Resting CBF neither -17.8 [CI:-71.9 36.2], 0.09, 0.51) nor remaining cortex 5.2 [CI:-3.9 14.2], 0.26). Conclusion We found correlation between high activation, indicating link impaired The impairment thinning hypometabolism, suggesting affecting vessel function very early pathology leading neurodegenerative disease.

Language: Английский

Citations

0

A medicine and food homology formula prevents cognitive deficits by inhibiting neuroinflammation and oxidative stress via activating AEA–Trpv1–Nrf2 pathway DOI
Mingjie Li, Jingyi Xu,

Hua-Yue Zhang

et al.

Inflammopharmacology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 21, 2024

Language: Английский

Citations

0