Increased oxidative stress is implicated in the pathogenesis of age-related neurodegenerative diseases. CoQ10 reduces oxidative stress and amyloid pathology and improves behavioral performance in the mouse models of Alzheimer’s disease. CoQ10 treatment decreases brain levels of protein carbonyls, a marker of oxidative stress. CoQ10 treatment resulted in decreased plaque area and number in hippocampus and […]
Emerging data suggest that improper signaling of the innate immune pathway at the synapse leads to pathological synapse loss in age-related neurodegenerative diseases. Phosphatidylserine is a class of phospholipids found in cell membranes. Its levels and location within the brain can affect important signaling pathways for cell survival and communication.
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Boosts the expression of brain-derived neurotrophic factor and nerve growth factor, increases synaptic plasticity and decreases the accumulation of amyloid β-protein. Has been shown to improve both spatial and non-spatial memory in aged mice.
Patients with cognitive dysfunction often have reduced levels of Vitamin E in the CSF. Vitamin E is a potent antioxidant which protects neuronal myelin sheets from oxidation. These neurons are necessary for communication between the brain and muscles cells for coordination of motion.
Inhibits antibody aggregation which reduces plaque formation; is an antioxidant and is anti inflammatory.
Inhibits antibody aggregation which reduces plaque formation; is an antioxidant and is anti inflammatory
Evidence indicates that SAM-e levels are lower in patients with Alzheimer’s, which may compromise their metabolism and brain function. SAM-e is involved in glutathione production, a powerful antioxidant that works from within the cell. SAM-e increases the turnover of serotonin and may increase levels of dopamine and norepinephrine. It’s been shown to exhibit anti-inflammatory and
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Zinc is critical in the enzymatic processing of the amyloid precursor protein (APP) and in the enzymatic degradation of the amyloid-β (Aβ) peptide. Intracellular organelles, transporters, and metal binding proteins sequester and release zinc to maintain balance between second messenger signaling, transcriptional regulation, and pathological increases in the ion.
