Turmeric Protects the Neurons Against Amyloid Plaques that Cause the Onset of Alzheimer’s disease

By Kyle J. Norton


Amyloid plaques are the formation of beta-amyloid, which has been found to interfere or disrupt the information transmitted between nerve cells.

Beta-amyloid, the main component of the amyloid plaques found in the brain cells is a hallmark in patients with Alzheimer's disease.

Beta-amyloid formed part of the larger protein called “amyloid precursor protein” (APP) that extends from the inside of brain cells to the outside by passing through the fatty membrane around the cell.

According to the statistics, from Alzheimer’s Disease International, nearly 44 million people worldwide, are living with Alzheimer’s or related dementia.

Sadly, Alzheimer’s and dementia is most common in Western Europe and North America compared to other parts of the world.

A joint study led by the Woosuk University, Wanju suggested that-5 ethanol extract including turmeric may have a therapeutic effect in vitro and in vivo on Aβ-induced AD in mice.

Under normal conditions, APP bind to other proteins on the surface of cells to attach to one another, when they are cut by other proteins. In some circumstances, probably due to DNA alternation or genetic mutation, one of the pieces beta-amyloid is produced. The accumulation of beta-amyloid into microscopic amyloid plaques over time can cause gradual death of the affected brain cell, leading to to the onset of Alzheimer’s disease (AD).

Turmeric is a perennial plant in the genus Curcuma, belonging to the family Zingiberaceae, native to tropical South Asia.

The herb has been used in traditional medicine as anti-oxidant, hypoglycemic, colorant, antiseptic, wound healing agent, and to treat flatulence, bloating, and appetite loss, ulcers, eczema, inflammations, etc.

According to the study, WS-5 exerted a significant inhibitory effect on acetylcholinesterase (AChE). associated with reduced function of neurotransmitters.

Furthermore, WS-5 prevented Aβ oligomerization associated with neurodegeneration in Alzheimer's disease via inhibition of Aβ 1-42 aggregation.

Moreover, according to the 1, 1-diphenyl-2-picrylhydrazyl (DPPH) assay, WS-5 possessed a high antioxidant activity, observed by the increase of the total antioxidant status (TAS).

Some researchers in the investigated the increased expression of amyloid plaques found in the aging population with AD wrote, "Age is the single greatest risk factor for Alzheimer’s disease with the incidence doubling every 5 years after age 65".

And, "a highly significant correlation between increasing age and slowed amyloid-beta turnover rates (2.5-fold longer half-life over five decades of age). In addition, we found independent effects on amyloid-beta42 kinetics specifically in participants with amyloid deposition. Amyloidosis was associated with a higher (>50%) irreversible loss of soluble amyloid-beta42 and a 10-fold higher amyloid-beta42 reversible exchange rate".

In other words, the genetic preposition that causes the onset of amyloid beta accumulation takes years to form amyloid plaques that destroy the brain neuron.

Additionally, WS-5 also protected the neuron against plaque formation by its anti-inflammatory properties observed by the inhibition of lipopolysaccharide-induced production of nitric oxide and two proinflammatory cytokines, TNF-α and IL-6, similarly to those in elderly AD.

More importantly, memory impairment in mice with Aβ-induced AD was also inhibited by the injection WS-5, according to the Morris water maze and passive avoidance test. 

In other words, W-5 protected the neurons against the pathological changes in the hippocampus and cortex region of the mouse brain induced AD by lipopolysaccharide.

More importantly, WS-5 (250 mg/kg) treatment improved learning and suppressed memory impairment as well as reduced Aβ plaque accumulation in Aβ-induced AD.

Collectively, researchers wrote, "WS-5 could be applied as a natural product therapy with a focus on neuroinflammation-related neurodegenerative disorders".

Taken altogether, turmeric processed abundantly bioactive compound curcumin may be considered supplements for the prevention of amyloid plaques induced neurodegenerative disorders, pending to the confirmation of the larger sample size and multicenter human study.

Intake of turmeric in the form of supplement should be taken with extreme care to prevent overdose acute liver toxicity.

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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.

Sources
(1) Synthetic Curcumin Analogs as Inhibitors of β -Amyloid Peptide Aggregation: Potential Therapeutic and Diagnostic Agents for Alzheimer's Disease by Bukhari SN1, Jantan I. (PubMed)
(2) WS-5 Extract of Curcuma longa, Chaenomeles sinensis, and Zingiber officinaleContains Anti-AChE Compounds and Improves β-Amyloid-Induced Memory Impairment in Mice by Kim JE1, Shrestha AC1, Kim HS1, Ham HN1, Kim JH1, Kim YJ1, Noh YJ1, Kim SJ1, Kim DK1, Jo HK2, Kim DS2, Moon KH3, Lee JH3, Jeong KO3, Leem JY. (PubMed)
(3) Age and Amyloid Effects on Human CNS Amyloid-Beta Kinetics by Bruce W. Patterson, PhD,1 Donald L. Elbert, PhD,2 Kwasi G. Mawuenyega, PhD,3 Tom Kasten, PhD,3 Vitaliy Ovod, MS,3 Shengmei Ma, MS,4 Chengjie Xiong, PhD,4,7 Robert Chott, BS,1Kevin Yarasheski, PhD,1 Wendy Sigurdson, RN, MSN,3,7 Lily Zhang, BS,8 Alison Goate, D. Phil,5,8 Tammie Benzinger, MD, PhD,6,7 John C. Morris, MD,3,7 David Holtzman, MD,3,7,8and Randall J. Bateman, MD. (PMC)