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7. Tyler, C. R., and A. M. Allan. The effects of arsenic exposure on neurological and cognitive dysfunction in human and rodent studies: a review. Current Environmental Health Reports 132–147, Report No. 2196-5412 (Electronic) (2014).

8. Basha, M. R., et al. The fetal basis of amyloidogenesis: exposure to lead and latent overexpression of amyloid precursor protein and beta-amyloid in the aging brain. Journal of Neuroscience 25: 823–829, doi: 10.1523/JNEUROSCI.4335-04.2005 (2005).

9. Bakulski, K. M., L. S. Rozek, D. C. Dolinoy, H. L. Paulson, and H Hu. Alzheimer’s disease and environmental exposure to lead: the epidemiologic evidence and potential role of epigenetics. Current Alzheimer Research 9: 563–573 (2012).

10. Ashok A., N. K. Rai, S. Tripathi, and S. Bandyopadhyay. Exposure to As-, Cd-, and Pb-mixture induces Aβ, amyloidogenic APP processing and cognitive impairments via oxidative stress-dependent neuroinflammation in young rats. Toxicological Sciences 143: 64–80, doi: 10.1093/toxsci/kfu208 (2015).

11. Dysken, M. W. et al. Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial. Journal of the American Medical Association 311: 33–44, doi:10.1001/jama.2013.282834 (2014).

12. Poole, S., S. K. Singhrao, L. Kesavalu, M. A. Curtis, and S. Crean. Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer’s disease brain tissue. Journal of Alzheimer’s Disease 36: 665–677, doi: 10.3233/JAD-121918 (2013).

13. Descamps, O., Q. Zhang, V. John, and D. E. Bredesen. Induction of the C-terminal proteolytic cleavage of AβPP by statins. Journal of Alzheimer’s Disease 25: 51–57, doi: 10.3233/JAD-2011-101857 (2011).

14. Bredesen, D. E. Inhalational Alzheimer’s disease: an unrecognized – and treatable – epidemic. Aging (Albany NY) 8: 304–313 (2016).

Глава 8: Протокол ReCODE: восстановление когнитивных функций

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6. http://www.drperlmutter.com/learn/resources/probiotics-five-core-species.

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8. http://www.survivingmold.com/shoemaker-protocol/Certified-Physicians-Shoemaker-Protocol

9. https://www.functionalmedicine.org/practitioner_search.aspx?id=80007.

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Приложение D

1. Galvan, V., et al. Reversal of Alzheimer’s-like pathology and behavior in human APP transgenic mice by mutation of Asp664. Proceedings of the National Academy of Science USA 103: 7130–7135, doi:10.1073/pnas.0509695103 (2006).

2. Там же.

3. Theendakara, V., et al. Neuroprotective sirtuin ratio reversed by ApoE4. Proceedings of the National Academy of Science USA 110: 18303–18308, doi: 10.1073/pnas.1314145110 (2013).

4. Lourenзo, F. C., et al. Netrin-1 interacts with amyloid precursor protein and regulates amyloid-beta production. Cell Death and Differentiation 16: 655–663, doi: cdd2008191 [pii]10.1038/cdd.2008.191 (2009).

5. Lu, D. C., et al. A second cytotoxic proteolytic peptide derived from amyloid-beta-protein precursor. Nature Medicine 6: 397–404, doi:10.1038/74656 (2000).

6. Spilman, P., B. Jagodzinska, D. E. Bredesen, and John Varghese. Enhancement of sAPPα as a therapeutic strategy for Alzheimer’s and other neurodegenerative diseases. HSOA Journal of Alzheimer’s & Neurodegenerative Diseases 1: 1–10 (2015).

7. Spilman, P. R., et al. Netrin-1 interrupts amyloid-beta amplification, increases sAβPPα in vitro and in vivo, and improves cognition in a mouse model of Alzheimer’s disease. Journal of Alzheimer’s Disease 52: 223–242, doi: 10.3233/JAD-151046 (2016).

8. Julien, O., et al. Unraveling the mechanism of cell death induced by chemical fibrils. Nature Chemical Biology 10: 969–976, doi: 10.1038/nchembio.1639 (2014).

9. Matrone, C., et al. Activation of the amyloidogenic route by NGF deprivation induces apoptotic death in PC12 cells. Journal of Alzheimer’s Disease 13: 81–96 (2008).

10. Bredesen, D. E. Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707–717, doi: 10.18632/aging.100690 (2014).

11. Bredesen, D. E., et al. Reversal of cognitive decline in Alzheimer’s disease. Aging 8: 1250–1258, doi: 10.18632/aging.100981 (2016).