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According to research, in 2020, as many as 5.8 million Americans were living with Alzheimer’s disease (AD). As a cancer survivor managing a long-term side effect called chemo brain, the prospect of future dementia, cognitive impairment, etc. is daunting.
First and foremost, its important to point out that as of today, conventional medicine can do little if anything about the aging person’s dementia much less about AD.
The solution then, in my experience anyway, are evidence-based but non-conventional, non-toxic therapies. I have spent years working to heal my chemo brain.
My definition of an evidence-based, non-conventional therapy is any therapy, supported by research (see below) but that is not approved by the Food and Drug Administration (FDA).
Not being studied and approved by the FDA is not a good or bad thing. Drug companies in my experience, don’t study any therapy than cannot be patented. That’s a product of a capitalist economy… For-profit organizations don’t spend resources about products were they cannot patient and sell.
This website, PeopleBeatingCancer.org, is filled with blog posts that cite nutrition, supplementation and lifestyle therapies that reduce the risk of dementia. The studies linked below take the discussion a step further by citing supplementation that effectively attacks AD.
Please be aware that these studies are in vivo aka their are animal studies, not human studies.
The bottom line, according to the research linked below, is that supplements Nattokinase, Serraptase and Curcumin all act against Alzheimer’s Disease.
If you would like to learn more about other AD therapies, scroll down the page, post a question or a comment. I will reply to you ASAP.
“Serrapeptase (SP) and nattokinase (NK) are proteolytic enzymes belonging to serine proteases. In this study, we hypothesized that SP and NK could modulate certain factors that are associated with Alzheimer’s disease (AD) pathophysiology in the experimental model.
Oral administration of aluminium chloride (AlCl3) in a dose of 17 mg/kg body weight (bw) daily for 45 days induced AD-like pathology in male rats with a significant increase in brain acetylcholinesterase (AchE) activity, transforming growth factor β (TGF-β), Fas and interleukin-6 (IL-6) levels.
Meanwhile, AlCl3 supplementation produced significant decrease in brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) when compared with control values. Also, AlCl3 administration caused significant decline in the expression levels of disintegrin and metalloproteinase domain 9 (ADAM9) and a disintegrin and metalloproteinase domain 10 (ADAM10) genes in the brain.
Histological investigation of brain tissue of rat model of AD showed neuronal degeneration in the hippocampus and focal hyalinosis with cellular as well as a cellular amyloid plaques formation. Oral administration of SP or NK in a rat model of AD daily for 45 days resulted in a significant decrease in brain AchE activity, TGF-β, Fas and IL-6 levels.
Also, the treatment with these enzymes produced significant increase in BDNF and IGF-1 levels when compared with the untreated AD-induced rats. Moreover, both SP and NK could markedly increase the expression levels of ADAM9 and ADAM10 genes in the brain tissue of the treated rats. These findings were well confirmed by the histological examination of the brain tissue of the treated rats. The present results support our hypothesis that the oral administration of proteolytitc enzymes, SP and/or NK, would have an effective role in modulating certain factors characterizing AD. Thus, these enzymes may have a therapeutic application in the treatment of AD.”
“Alzheimer’s disease constitutes a growing cause of cognitive impairment in aging population. Given that current treatments do not produce the desired therapeutic effects, the need for finding alternative biological and pharmacological approaches is critical.
Accumulating evidence suggests inflammatory and oxidative stress responses as potential causal factors of cognitive impairments in Alzheimer’s disease and healthy aging.
Curcumin has received increased interest due to its unique molecular structure that targets inflammatory and antioxidant pathways as well as (directly) amyloid aggregation; one of the major hallmarks of Alzheimer’s disease.
Therefore, this review summarizes preclinical and clinical findings on curcumin as a potential cognitive enhancer in Alzheimer’s disease and normal aging. Databases used for literature searches include PubMed, EMBASE and Web of Science; in addition, clinicaltrials.gov was used to search for clinical studies.
Overall, animal research has shown very promising results in potentiating cognition, both physiologically and behaviourally.
However, human studies are limited and results are less consistent, complicating their interpretation. These inconsistencies may be related to differences in methodology and the included population. Taking into account measurements of important inflammatory and antioxidant biomarkers, optimal dosages of curcumin, food interactions, and duration of treatment would increase our understanding on curcumin’s promising effects on cognition. In addition, increasing curcumin’s bioavailability could benefit future research…”