A Natural Treatment for Alzheimer's disease (AD) with No Side Effects

By Kyle J. Norton

Ginger may be the next pharmaceutical target to extract a single ingredient medicine for the treatment of Alzheimer’s disease, some scientists found.

Alzheimer’s disease is a common neurodegenerative disease in the elderly characterized by slowly destroys memory and thinking skills and, eventually, the ability to carry out the daily tasks.

 

According to the to the Centers for Disease Control and Prevention (CDC), Alzheimer’s disease falls sixth on the list of leading causes of death in the United States.

The average time from diagnosis to death was about four years.

 

Alzheimer’s disease is also increased with the increase in age. In the total of 2,566 people, ages 65 and older under the test of dementia, 559 participants without dementia at the start of the study developed Alzheimer’s disease.

 

Most common causes of Alzheimer’s disease are the combination of genetic, lifestyle, and environmental factors.

 

However, aging is one most risk factors associated with the onset of the disease in the elderly. Statistics show, the number of people with the disease doubles every 5 years beyond age 65. About one-third of all people age 85 and older may have Alzheimer’s disease.

 

Some researchers suggested that the increase in age and risk of Alzheimer’s disease can be attributed to the shrinking of certain parts of the brain, and long-term low-grade inflammation, neuron damage induced by oxidative stress due to overexpression of free radicals.

 

Dr. Tuppo EE, the lead author of the neuro team at the Western University of Health Sciences said, “There is increasing evidence that free radical-induced oxidative damage may play a role in the pathogenesis of Alzheimer’s disease. Free radicals are reactive oxygen compounds that may attack and damage lipids, proteins, and DNA”.

And, “The brain is especially sensitive to oxidative damage because of its high content of readily oxidized fatty acids, high use of oxygen, and low levels of antioxidants”.

 

These results clearly suggested that people who follow a healthy diet with high antioxidants such as fruits and vegetables, whole grain and fewer in red meat and processed foods may have a substantially lower risk of Alzheimer’s diseases.

Ginger (Zingiber officinale) or ginger root, the second superfood used for thousands of years by mankind, is the genus Zingiber, belonging to the family Zingiberaceae, native to Tamil.

The root has been used in traditional and Chinese medicine to treat dyspepsia, gastroparesis, constipation, edema, difficult urination, colic, etc.

On finding the natural ingredient and whole food with a potential effect on patients with Alzheimer’s disease, researchers looked into Ginger (Zingiber officinale), a common dietary adjunct that not contributes to the taste and flavor of foods, but also contain a number of potentially bioactive phytochemicals having valuable medicinal properties.

 

The differentiation of the binding interactions between active ginger components and various anti-Alzheimer drug targets, researchers suggested the approach could be a promising computational tool to aid optimization of lead compounds obtained from the ginger.

The hydrophobic/hydrophilic interactions of ligands isolated from ginger showed to target acetylcholinesterase, the functioning neurotransmitters, and receptors c-Jun N-terminal kinase which plays an important role in the onset of cognitive impairment.

 

Additionally, researchers found that all isolated compound is satisfied the Lipinski’s rule of five, making them potentially promising drug candidates for the treatment of Alzheimer’s disease.

 

Where Lipinski’s rule of five is simply the rule of five (RO5) is a rule to determine if a chemical compound with a certain pharmacological or biological activity has chemical properties.

 

Moreover, the in-depth investigation of the possible mechanisms of action of these compounds against the AD, scientists compared 4 bioactive compounds isolated from ginger to inhibitors of human acetylcholinesterase (HssAChE), the HssAChE inhibitor and commercial drug in use against the AD, donepezil (DNP).

 

Unsurprisingly, two among the compounds studied: (E)-1,7-bis(4-hydroxy-3-methoxyphenyl) hept-4-en-3-on and 1-(3,4-dihydroxy-5-methoxyphenyl)-7-(4-hydroxy-3- ethoxyphenyl) heptane-3,5-diycl diacetate, are considered promising new HssAChE inhibitors that could be as effective as DNP.

 

Based on these results, researchers said, “the binding of the studied compounds in the different binding pockets inside HssAChE and established the preferred interactions to be favored in the design of new and more efficient inhibitors”.

 

Taken altogether, ginger processed abundant bioactive compounds that act as acetylcholinesterase (HssAChE) inhibitor may be used as a functional food for the prevention and treatment of Alzheimer’s disease without inducing any side effects.

 

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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 ISSN 0975-6299.

Sources
(1) Ginger components as new leads for the design and development of novel multi-targeted anti-Alzheimer’s drugs: a computational investigation by Azam F1, Amer AM2, Abulifa AR2, Elzwawi MM2. (PubMed)
(2) A molecular dynamics study of components of the ginger (Zingiber officinale) extract inside human acetylcholinesterase: implications for Alzheimer disease by Cuya T1, Baptista L2, Celmar Costa França T. (PubMed)
(3) Ginger fermented with Schizosaccharomyces pombe alleviates memory impairment via protecting hippocampal neuronal cells in amyloid beta1-42 plaque injected mice by Huh E 1, Lim S , Kim HG , Ha SK , Park HY , Huh Y , Oh MS. (PubMed)