HupA or HuperineA a Chinese moss grown indigenous to south east Asia, is water soluble perennial alkaloid with very unique properties with a dosage half life of 10-14 hours.
HupA has been used for more than a thousand years for various treatments and number of ailments such as nerve agents, insecticides, organophosphate poisoning and schizophrenia. Since then HupA’s been extensively researched by Chinese researchers for bio-activity, especially for bioactivity toward cholinesterase a potential treatment for Alzheimer’s Disease and reducing free radical activity while enhancing neighboring antioxidants. In 1996 HuperzineA began being sold as Huperzine Serrata Leaf as a tablet called “ Shuangyiping “ as a drug for symptomatic AD thus began being marketed in the U.S in it’s HupA powder form after it was discovered not only treat symptomatic AD, but significantly improved memory deficits within the elderly and showed improvement of patients with vascular dementia and suffering from benign senescent forgetfulness with minimal peripheral colinergic side effects.
Vascular Dementia (VaD) is associated with the cerebrovascular brain it can be viewed as a larger syndrome of vascular cognitive impairment.
Main trial results of HupA on (VaD)
‘ We included only one small trial, involving 14 participants with vascular dementia. No significant effect of Huperzine A on cognitive function measured by MMSE (WMD 2.40; 95% CI −4.78 to 9.58) was observed. There was a significant beneficial effect of Huperzine A on performance of activities of daily living (WMD −13.00; 95% CI −23.24 to −2.76) after six months of treatment. No deaths from any cause at the end of treatment were reported. Behaviour, quality of life and caregiver burden were not assessed in the included trial.‘
No deaths still sounds pretty nice for a simple moss as a treatment.
The inhibitory effects of HupA on is selective with degrading the (AChE) over Butyrycolinesterase (BChE) because it can easily pass through the blood brain barrier ( BBB) Acetycholinesterase (AChE) which is the enzyme that breaks down the neurotransmitter Acetoycholine, the break down is prevented by HupA locking into a deep chasm or “ active gauge site “ which funnels the Acetylcholine down into the AChE where it’s broken down prior to being cycled. The results of this process are optimized cognition and greater
HupA also has shown to resist Beta Amyloid induced dysfunction, Beta Amyloid are the main constituents of Amyloid plaques that are found in the brains of Alzheimer’s patients. Beta Amyloid reduces the amount of ATP within mitochondria and low cellular energy production and shields against associative complication that would follow one of many being type II diabetes which is projected to claim 3,000,000 lives annually heading to the year 2030. The HupA input carries neuroprotective mechanisms as well, antagonizing the NMDA receptor protects against onset Glutmate induced cell death, but also decreased glutamate induced calcium mobilization which entails a degradation of neurons because of the antagonization may be beneficial for the excitatory amino acid overestimulation seen in ischemia which is the restriction of blood flow.
The neurofactor of HupA however has interesting protocol which stimulates the growth of new dendrites, these are the branch extension of a nerve cell along which the impulses are transmitted from one neuron to another. Stronger signals means more neuronal networks, a strong enhancement in recall and neuroplasticity.
Since HupA has half life of about 14 hours, it isnt recommend to take daily, dosages range from 50-200mcg. Since it’s water soluble the effects are immediate.