According to the National Dementia Epidemiology Survey in 2012, the prevalence of dementia in elderly people aged 65 and over is 9.18%, and AD patients account for 70.5% of all dementia patients. In addition, the distribution of severity of dementia according to the degree of dementia and the degree of total dementia accounted for 58.8% of the total. The prevalence of mild cognitive impairment was 27.82%, which is estimated to be over one-quarter of the total elderly population over 65 years of age.
Most of the drugs currently marketed as Alzheimer's drugs are acetylcholinesterase inhibitors that inhibit the degradation of acetylcholine, a neurotransmitter that is very important for memory function. Acetylcholinesterase inhibitors are drugs that focus on symptom relief rather than cause cure. Major side effects include excessive exacerbation of acetylcholine, which is known to exacerbate parasympathetic nervous system and to exacerbate digestive and neuropsychiatric disorders such as severe diarrhea, nausea, vomiting, depression, anxiety, insomnia, headache, Because of these side effects, we are not able to use drugs that are currently on the market at the time when memory loss begins (mild cognitive impairment, AD). Therefore, there is no drug that can treat early AD patients, and drug development that is able to treat the underlying cause of illness rather than symptom relief and low side effects is urgently needed.
Moriah 1000 (M1K) is a natural peptide substance that shows learning and memory recovery effects. This effect of Moriah 1000 is because it regulates the signaling pathway of RAGE, a receptor that transports beta-amyloid (Aβ) peptide into the brain, which induces brain cell death and is known to be a risk factor for AD. Moriah 1000 binds to raises and blocks beta amyloid from entering the brain, thereby inhibiting the formation of amyloid plaques in the brain and blocking the progressive signaling pathway of beta amyloid binding to raises, thus preventing the brain's primary immune system, BBB) to prevent damage and inhibit inflammation and nerve cell death in the brain to prevent disease progression, learning and memory recovery effect.