Herbal Formula Purges Deadly Proteins From Brain

Neurodegenerative disease, including Alzheimer’s disease, is the fastest-growing cause of death in the world. Traditional Chinese medicine may offer hope.

Pharmaceutical companies have wasted billions of dollars in pursuit of drugs that can treat prion disease (which includes Alzheimer’s disease). For decades, the hunt for a cure has focused on a deadly protein called beta-amyloid, which builds up in the brain.

Currently available treatments offer only moderate symptomatic relief. Effective, safe therapies and/or drugs are needed. The key hallmark features of AD are: loss of cholinergic neurons; tau-associated neurofibrillary tangles (NFTs) and accumulating amyloid β-peptide (Aβ) generates senile plaques (SP) derived from amyloid precursor protein.

Aβ and NFTs are well correlated with cognitive impairment. Research on mice determined that there is a metabolic link between Aβ and tau. Tackling Aβ and NFTs together seems to be a better strategy than targeting tau alone. Alzheimer drugs today relieve some symptoms, but are not cures for neurodegenerative disease. Unfortunately, most trials of anti-amyloid treatments have repeatedly failed, but researchers in China hope to reverse that trend.

A new Chinese medicine called NeuroDefend promotes anti-Aβ and anti-tau effect in experimental Alzheimer’s disease (AD) models.

Researchers from the School of Chinese Medicine at Hong Kong Baptist University (HKBU) developed NeuroDefend by combining six Chinese herbal medicines. Experiments on mice showed that the formula reduces the levels of amyloid-beta (Aβ) and tau protein, which are the major hallmarks of AD, in mice brains. It also improves cognitive function and memory in mice. The research was published in the Journal of Food and Drug Analysis, an international scientific journal.

AD is characterized by a collection of abnormal proteins in the brain, which cause inflammation and a deadly cascade of events, including the rapid loss of brain cells. Parkinson’s disease is essentially the same disease, but the symptoms are different because a different region of the brain is eroding. Preventing this accumulation of proteins in the brain appears to be a critical success factor for successful treatment. It appears that the Chinese research team is on target.

NeuroDefend was developed by a team led by Li Min, Professor of the Teaching and Research Division and Associate Dean of the School of Chinese Medicine at HKBU. The researchers found that Huang-Lian-Jie-Du-Tang (HLJDT), a traditional Chinese herbal formula comprised of Huang Lian, Huang Qin, Huang Bai and Zhi Zi that is used to treat cerebral ischemia, could significantly reduce Aβ levels in mouse models when Huang Qin was removed. They also found that Yan Hu Suo in Yuan-Hu Zhi Tong (YZT), a Chinese herbal formula used to treat pain and neuralgia, can regulate the aggregation of tau proteins. They therefore combined the modified HLJDT (HLJDT without Huang Qin) and Yan Hu Suo with two other herbal medicines, namely Dan Shen and Gou Teng, to optimize the formula for AD treatment.

traditional Chinese medicine treats Alzheimer's disease

“Traditional Chinese medicine adopts a broad pharmacological approach to treating neurodegenerative diseases by deploying a combination of herbal medicines with different treatment effects. Selection of the six herbal ingredients and their ratios in NeuroDefend is based on the research conducted by our team over the years. NeuroDefend will contribute to the development of novel, effective traditional Chinese medicine for the treatment of AD in humans,” said Professor Li.

In the pre-clinical experiments, 50 mice in the treatment group were orally given low, medium and high daily dosages of NeuroDefend for three or eight months. Another 40 mice were put in the control group. The results showed that Aβ levels and abnormal tau protein aggregation in the treatment group were both significantly reduced by 30 to 40 percent. The higher dosage was found to be more effective in reducing Aβ levels and abnormal tau protein aggregation.

To evaluate the efficacy of NeuroDefend in improving cognitive behaviours and memory deficits, a water maze experiment was conducted. Mice were trained to swim to a platform and remember its position in a water pool. After the platform was removed, researchers observed whether the mice were able to recall and approach the original position of the platform. Compared to the control group, mice treated with NeuroDefend stayed 18 to 25 seconds longer probing for the platform’s original position. This showed the efficacy of the formula in improving the memory and learning ability of the mice with AD.

In another experiment, mice were exposed to an audio tone followed by a two-second electric shock to their feet from the floor of the chamber. When they were put back into the chamber the next day without any electric shock, the mice were seen to “freeze” their body movements due to the fear of an electric shock. The freezing duration of the mice treated with NeuroDefend was 70 to 80 seconds longer than that of the control group. It demonstrated that the mice treated with NeuroDefend remembered the shock, reflecting the efficacy of the formula in improving their memory deficits.

Currently, medications for AD offer moderate symptomatic relief but fail to cure the disease; hence development of effective and safe drugs is urgently needed for AD treatment. In this study, we investigated a Chinese medicine (CM) formulation named NeuroDefend (ND), for reducing amyloid β (Aβ) and tau pathology in mice. Regular oral administration of ND improved cognitive function and memory in 3XTg-AD and 5XFAD mice. In addition, ND reduced beta-amyloid precursor protein (APP), APP C-terminal fragments (CTF-β/α), Aβ and 4G8 positive Aβ burden in 3XTg-AD and 5XFAD mice. Furthermore, ND efficiently reduced the levels of insoluble phospho-tau protein aggregates and AT8 positive phospho tau neuron load in 3XTg-AD mice. Hence, ND could be a promising candidate for the treatment of AD in humans.

LaFerla and his group were the first to generate the 3XTg-AD mouse model, which is generally used in drug screening and drug discovery. This transgenic mice models express mutated APP, tau protein (APPswe and TauP301L respectively), and mutated PS1 protein (PS1M146V), which develop both NFTs and amyloid plaques. Interestingly, 3XTg-AD mice exhibited a phenotype of Aβ and NFTs pathology affecting synaptic plasticity, which impairs long-term potentiation and memory.

An ideal drug for AD would reduce both Aβ and NFTs. Which is why current research focuses on these essential aspects. Traditional Chinese Medicine (TCM), an ancient and effective medicinal system extensively used in East Asia, uses this type of combinational approach, with multiple herbal extracts for addressing various aspects of a medical condition simultaneously. Today, TCM is used for the treatment of several neurological diseases including AD. TCM herbs are attracting wide attention for drug discovery and therapeutic approaches. Since ND formulation is composed of several active compounds, their mechanism of action for AD therapy will be studied in the future. In the future, ND could be developed as a health food supplement, or its raw materials could be used as medicine to prevent or treat AD.

There is no cure for prion disease, which claims millions of lives of all ages every year. This pandemic has been surging around the globe for the past 40 years. The pandemic is so prevalent and mismanagement so negligent, that the scourge has spread to wildlife, livestock and sea mammals.

treat Alzheimer's disease

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Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy.