According to WHO, currently, more than 55 million people live with dementia worldwide, and there are nearly 10 million new cases every year. The most common type (60-70%) of dementia is Alzheimer’s disease (AD), a progressive disease characterized by memory loss, language breakdown, and eventually, death. The main pathological factor for AD is thought to be the progressive accumulation of amyloid beta (Aβ) peptides in the brain, generated by the cleavage of the amyloid precursor protein (APP) by a combination of β-secretases and γ-secretases. Hyperphosphorylation of tau, a microtubule-associated protein which aggregates to form tangles, also damages the brains of patients with AD.

This year, we’re excited to announce that ANKASCIN^® 568 product has successfully received a health certificate for “Anti-aging” Support. SunWay research demonstrates the protective effect of ANKASCIN^® 568 in 4 aging models:

Amyloid β-Infused Rats

In this study, the effects of dietary administration of ANKASCIN^® 568 on memory and learning abilities are confirmed in an animal model of AD rats infused with Aβ₄₀ into the cerebral ventricle. During continuous Aβ40 infusion for 28 days, ANKASCIN^® 568 administration potently reverses the memory deficit in the memory task. Aβ₄₀ infusion increases acetylcholinesterase activity, reactive oxygen species, and lipid peroxidation and decreases total antioxidant status and superoxide dismutase activity in brain, but these damages were potently reversed by ANKASCIN^® 568 administration. The protection provided by ANKASCIN^® 568 is able to prevent Aβ fibrils from being formed and deposited in hippocampus and further decrease Aβ₄₀ accumulation, even though Aβ₄₀ solution was infused into brain continuously.

Aluminum-induced AD rats

We examined the effects of ANKASCIN^® 568 in the model of Sprague–Dawley rats via oral garage to induce AD pathology which received aluminum chloride on a daily basis. ANKASCIN^® 568 mitigated cognitive impairment in behavioral tests, reduced oxidative stress in the brain, reversed aluminum-induced AD brain pathology including accumulation of Aβ, p-tau, and APP; elevated acetylcholinesterase activity, and altered biomarker levels in the cerebrospinal fluid.

Juglone-induced C. elegans

Researchers found out that monascin (MS) increased the survival of Caenorhabditis elegans under juglone-induced oxidative stress, and attenuated endogenous levels of reactive oxygen species and Aβ deposit. In addition, mRNA levels of strain CL4176 of several antioxidant genes (sod-1, sod-2, sod-3, hsp16.2) and daf-16 were up-regulated by MS treatment. The findings suggest that MS can be used for the prevention of AD-associated oxidative stress.

J20 APP Transgenic Mice

This study investigated the bioactive functions of ankaflavin (AK) and monascin (MS) in the fermented product of ANKASCIN^® 568 and found their abilities to ameliorate AD by modifying several important pathogenic factors including improved cognitive function, reversed behavioral deficits, reduced hippocampal Aβ burden, decreased tau hyper-phosphorylation, and reduced neuroinflammation in the J20 mouse model of AD.

To confirm the effect of ANKASCIN^® 568 on improving the learning and memory ability of AD individuals, a clinical trial was conducted:

Clinical trial

After 18 months of the experimental period, ANKASCIN^® 568 shows positive results in AD subjects in the Mini-Mental State Examinations, Distress Scale, and Emotional Behavior Scales because of the significant effect on memory and learning ability.

With the global population getting older and an increasing number of over 50’s in every country, the demand for anti-ageing nutritional solutions has risen sharply in recent years. This year, we’re excited to announce that ANKASCIN^® 568 product has successfully received a health certificate for Anti-aging Support from the government. It is believed that we can bring you better product value and make you more accessible on the road to healthy aging.

For more information, please get in touch with us: globalservice@sunway.cc

Reference:

Red mold rice ameliorates impairment of memory and learning ability in intracerebroventricular amyloid β-infused rat by repressing amyloid β accumulation. (link)

Monascus purpureus NTU 568 fermented product improves memory and learning ability in rats with aluminium-induced Alzheimer’s disease. (link)

Monascin from Monascus-fermented products reduces oxidative stress and amyloid‑β toxicity via DAF-16/FOXO in Caenorhabditis elegans. (link)

Monascus purpureus fermented product ameliorates learning and memory impairment in the amyloid precursor protein transgenic J20 mouse model of Alzheimer’s disease. (link)

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