3.2 Preclinical studies of ferroptosis in neurodegenerative diseases 3.2.1 Ferroptosis and alzheimers disease AD is a prevalent and progressive neurodegenerative disorder, characterized by the accumulation of extracellular -amyloid (A) plaques and intracellular neurofibrillary tangles formed by hyperphosphorylated Tau protein, accompanied by excessive neuroinflammation, synaptic dysfunction, and neuronal loss, ultimately resulting in impairments in language, judgment, and executive function, and even leading to the loss of independent living ability ( 1-42 stimulation markedly suppressed the activation of the bone morphogenetic protein 6 (BMP6)/SMAD1 signaling pathway in BV2 microglial cells, resulting in the downregulation of SLC7A11, GPX4, FTL1, and FTH1 expression, increased ROS and MDA levels, and decreased GSH and SOD levels
This points to something researchers are calling a microbiota-endocannabinoid axis
The preservative load suppresses these inputs but eventually depletes against repeated insults
Labs through Labcorp or Quest are recommended but not required to start
Lifestyle-based supplements (DHEA in some cases of low ovarian reserve) are used judiciously and under specialist supervision
Moreover, it has been suggested that starvation reduces liver glycogen storage and hence reduces UGT conjugative ability leading to a greater fraction of the dose being oxidised to NAPQI [77]
