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Why There’s No “One-Size-Fits-All” Cure for Alzheimer’s

Alzheimer’s is making headlines in the press at the moment due to Big Pharma’s trail of disappointing experimental drugs trials that failed to show benefit. After doing lot of in-depth research on the subject, I have both good and bad news for you.

Let’s start with the bad.

We traditionally thought that Alzheimer’s is a disease of “old age” but new research is showing that younger and younger people are affected with the condition or start developing neuropathologies associated with it.

For instance, a 2015 study microscopically examined the postmortem brains of 154 people aged 30-50 years for specific Alzheimer lesions (beta-amyloid plaques, neurofibrillary tangles, and tau-positive neurites) and found that beta-amyloid deposits in the cerebral cortex appear as early as 40 years of age in APOE4 carriers (1), APOE4 being the gene that predisposes one to the disease (2).

An even more alarming study published at the end of last year found that all children in Mexico City exhibit early signs of Alzheimer’s as defined by subcortical pretangles and cortical tau pre-tangles, and this was linked to air pollution (3).

These two studies looked at the brains of adults and children that displayed no overt sign of the disease. This is due to the fact that Alzheimer’s has a silent, asymptomatic stage during which people are cognitively intact despite having substantial pathologic changes in the brain.

Regarding genetic predisposition, what is interesting is that the dreaded ApoE4 gene (which all humans had 7 million years ago, ApoE3 and ApoE2 being recent mutations that appeared 220,000 and 80,000 years ago respectively) accounts only for 65% of cases, the other 35% being due to environmental factors. As an aside, the genesis of any disease, except for certain infectious illnesses, is always attributable to the fine interplay between genetics and the environment.

Another Alzheimer’s fact is that women are at the epicentre of this epidemic (4). If you’re a woman today your chance of getting Alzheimer’s has now exceeded your chance of getting breast cancer. In the US alone, women represent 65% of the patients and also 60% of the caregivers.

Moreover, it appears that the focus of Alzheimer’s research so far has been just plain wrong, in the sense that the amyloid-beta plaques are the cause but a consequence of the disease process, thus removing them would not stop neurodegeneration.

The good news is that there is an increasing amount of research that points to key biomolecular mechanisms that could be harnessed in order to prevent, stop and reverse neurodegeneration. Current strategies include modulating microglia astrocytes that constitute the brain’s immune system (5, 6) to ways of protecting healthy brain cells from neurotoxins and heavy metals such as lead, that we knew about for a long time (7).

One of the latest revelations in Alzheimer’s research in comes from a recent study published in the journal Nature Neuroscience which concludes that Alzheimer’s is caused by an accumulation of damaged mitochondria in the brain as a consequence of impaired mitophagy (8).

Mitophagy is the cell’s self-cleaning system that selectively degrades dysfunctional mitochondria, the energy-producing factories within cells, by a process known as autophagy (literally “self-devouring”). The study shows that stimulating mitophagy reverses memory impairment in animal models of the disease. This was done using mitophagy-inducing compounds, such as NAD+ precursors, urolithins and actinonin, which are all naturally occurring molecules (9, 10, 11) that can be enhanced with diet and nutrition as well as microbiome-manipulation strategies (more about dietary strategies to prevent or reverse early stage Alzheimer’s in a future article).

Going back to autophagy — the highly-regulated mechanism of the cell that disassembles unnecessary or dysfunctional components and recycles them — it has to be stated that the concept is not new, having been intuitively applied for thousands of years in traditional natural medicine systems and even religious rituals, in the form of fasting. However, it was only in 2016 that a Japanese researcher, Dr Yoshinori Ohsumi, discovered the genetic mechanism for autophagy and was awarded the Nobel Prize for it (12).

Last but not least, a number of MDs working in the Functional Medicine space have developed integrated approaches to reversing cognitive decline that focus on dietary and lifestyle interventions (13). In his 2016 presentation “Reversing Alzheimer’s Disease” that took place at Silicon Valley Health Institute, Dr. Dale Bredesen delineated a strategy focusing on the key physiological parameters that need to be addressed in order to reverse cognitive decline: hormone imbalances (14), deficiency of trophic factors (15), impaired glucose metabolism(16), neuroinflammation(17), sleep (18), exercise (19). His stance on the subject is very clear: Alzheimer’s is a complex chronic condition that cannot be targeted with a monotherapy. Instead, a multi-level programmatic approach is necessary.

In light of these recent discoveries and novel integrated approaches to tackling chronic degenerative illnesses, it shouldn’t surprise us anymore that Big Pharma failed to come up with the “magic pill” for Alzheimer’s. It is now clear that this was an impossible task to begin with. In a future article, we will present some of the dietary and lifestyle strategies that have already been found to greatly benefit patients with early-stage Alzheimer’s as well as improve brain health in everyone.

This is part of an ongoing series on maintaining good Brain Health. Read part 2 now!


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(2) Kim J, Basak JM, Holtzman DM (2009) The role of apolipoprotein E in Alzheimer’s disease. Neuron;63(3):287–303

(3) Calderón-Garcidueñas, Lilian, et al. (2018) Non-Phosphorylated Tau in Cerebrospinal Fluid is a Marker of Alzheimer’s Disease Continuum in Young Urbanites Exposed to Air Pollution. Journal of Alzheimer’s Disease, vol. 66, no. 4, pp. 1437-1451

(4) Podcasy JL, Epperson CN. (2016) Considering sex and gender in Alzheimer disease and other dementias. Dialogues Clin Neurosci.;18(4):437–446.

(5) Cao W. et al (2018) Peripheral immune system in aging and Alzheimer’s disease. Mol Neurodegener.;13(1):51

(6) Andreasson KI, Bachstetter AD, Colonna M, et al. (2017) Targeting innate immunity for neurodegenerative disorders of the central nervous system. J Neurochem. 2017 Apr;141(1):151

(7) Olson L, et al. (1984) Some toxic effects of lead, other metals and antibacterial agents on the nervous system–animal experiment models. Acta Neurol Scand Suppl. ;100:77-87.

(8) Evandro F. Fang, et al. (2019) Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease. Nature Neuroscience volume 22, pages 401–412

(9) Strømland Ø et al. (2019) Keeping the balance in NAD metabolism. Biochem Soc Trans. 2019 Feb 28;47(1):119-130

(10) Muku GE,et al. (2018) Urolithin A Is a Dietary Microbiota-Derived Human Aryl Hydrocarbon Receptor Antagonist. Metabolites;8(4):86. Published 2018 Nov 29

(11) Chen DZ et al (2000) Actinonin, a naturally occurring antibacterial agent, is a potent deformylase inhibitor. Biochemistry. Feb 15;39(6):1256-62.

(12) Ke PY. (2017) Horning cell self-digestion: Autophagy wins the 2016 Nobel Prize in Physiology or Medicine. Biomed J.;40(1):5–8

(13) Bredesen DE. (2014) Reversal of cognitive decline: a novel therapeutic program. Aging (Albany NY).;6(9):707–717

(14) Lan YL, Zhao J, Li S. (2014) Update on the Neuroprotective Effect of Estrogen Receptor Alpha Against Alzheimer’s Disease. J Alzheimers Dis.

(15) Lourenco FC et al. (2009) Netrin-1 interacts with amyloid precursor protein and regulates amyloid-beta production. Cell Death Differ.;16:655–663

(16) Yang Y, Wu Y, Zhang S, Song W. (2013) High glucose promotes A beta production by inhibiting APP degradation. PLoS One. 8:e69824

(17) Sutinen EM, et al. (2012) Pro-inflammatory interleukin-18 increases Alzheimer’s disease-associated amyloid-beta production in human neuron-like cells. Journal of neuroinflammation;9:199.

(18) Wade AG, et al. (2014) Add-on prolonged-release melatonin for cognitive function and sleep in mild to moderate Alzheimer’s disease: a 6-month, randomized, placebo-controlled, multicenter trial. Clin Interv Aging.;9:947–961

(19) Cotman CW et al.(2007) Exercise builds brain health: key roles of growth factor cascades and inflammation. Trends Neurosci.;30:464–472