Alzheimer's disease (AD) is a disease caused by progressive brain cell degeneration that accounts for 55-70% of all dementia. The prevalence of dementia in elderly people over 65 years old in the United States is 11% in 2014, reported to occur one AD every 67 seconds, and predicts that by 2050, one AD every 33 seconds, about 1 million new AD patients will be born each year.
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 disease 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, dementia). 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.
Moriah1000 (M1K) is a synthetic peptide substance that has learning and memory recovery effects. Such effects of Moriah 1000 are due to the regulation the signal pathway of RAGE, a receptor that transports beta-amyloid (Aβ) peptide, which is known to induce brain cell death and be a risk factor of AD, into the brain. Moriah 1000 binds to RAGE and blocks β-amyloid from entering the brain, inhibiting the formation of amyloid plaques in the brain and blocking the signal pathway that progresses as β-amyloid binds to RAGE, thus preventing the brain's primary immune system blood-brain barrier(BBB) and suppressing inflammation in brain and nerve cell death to prevent disease progression and show learning and memory recovery effects.