Patients with Alzheimer's disease show a reduced capacity of peripheral blood mononuclear cells/macrophages to phagocytose beta-amyloid, which returns to normal following the Bredesen protocol.
"there's some nice work out of UCLA years ago and continuing on, showing that if you simply look at your peripheral blood mononuclear cells, so you're looking at the ability of these monocytes and essentially macrophages, blood-borne macrophages, to chew up beta amyloid, to take it up, phagocytose it. Everybody with Alzheimer's has a reduced ability to do that. And when they actually go on the protocol we just published, that actually comes back to normal." (said at 0:24:10)
Research from UCLA (such as work by Fiala and colleagues) demonstrated that peripheral blood monocytes/macrophages from patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI) display impaired phagocytosis and clearance of amyloid-beta compared to healthy controls. However, the speaker's claim that amyloid phagocytosis in 'everybody with Alzheimer's' 'comes back to normal' following the protocol is overstated. Published studies co-authored with this group evaluating nutritional supplementation regimens (omega-3 fatty acids, antioxidants, and lifestyle measures) are very small, open-label, uncontrolled pilot studies. In one study (PMID 25805829), monocyte phagocytosis of amyloid-beta increased significantly in patients with minor cognitive impairment or pre-MCI, but the change in patients with established AD was not statistically significant.
- supports: Ineffective phagocytosis of amyloid-beta by macrophages of Alzheimer's disease patients. (Journal of Alzheimer's disease : JAD 2005)
"Control monocytes display excellent differentiation into macrophages and intracellular phagocytosis of Abeta followed by beta degradation or export. AD monocytes show poor differentiation and only surface uptake of Abeta and suffer apoptosis... In AD, however, macrophage phagocytosis is defective, which may elicit compensatory response by the adaptive immune system." (abstract, results and conclusions, passage verified)
pubmedfull study (doi) - partial: ω-3 Supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with mino… (FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2015)
"In patients with MCI and pre-MCI, phagocytosis of Aβ by monocytes increased from 530 to 1306 mean fluorescence intensity units (P = 0.016). The increase in patients with AD was not significant (N.S.)." (abstract, results, passage verified)
pubmedfull study (doi) - context: Increased intermediate M1-M2 macrophage polarization and improved cognition in mild cognit… (FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2017)
"Aβ 1-42 phagocytosis increased in both ApoE groups (P = 0.03 in each groups)... The validity of this study is limited by its small size and uncontrolled design." (abstract, results and conclusions)
pubmedfull study (doi)