1. Tracie Wymer Julie Franks Shirin Malek Inflammatory Diseases

2.  A substance purified from the Chinese club moss Huperzia Serrata  During the 1980s, investigators in China determined that huperzine A is a potent inhibitor of acetylcholinesterase (AChE)  Has been widely used in China for centuries in the treatment of contusions, strains, swelling and schizophrenia  Bioavailability: quickly absorbed by the brain

3. Alkaloid compound By mouth: doses of 50-200 mcg twice daily depending on the brand

4.  Huperzine A inhibits the activity of AChE.  Breakdown of acetylcholine is slowed and the strength and duration of the nerve impulse is improved.  Regulating B-amyloid precursor protein (APP) metabolism, protecting against AB-mediated oxidative stress, apoptosis and mitochondrial dysfunction as well as anti-inflammation.  Better brain functioning  Three FDA approved AChEIs for AD therapy include: donepezil, rivastigmine and galanthamine.

5.  Alzheimer’s and dementia patients have significantly low levels of acetylcholine.  ACh is the most abundant and essential neurotransmitter in the brain that is responsible for numerous functions, including cognition and memory.  Acetylcholinesterase (AChE) is an enzyme that breaks down ACh  Loss of ACh function is a primary feature of several types of brain dysfunction, including Alzheimer's disease

8.  Helps memory loss and boosts brain function  Helps prevent the breakdown of key neurotransmitters in the brain  Reduces oxidative damage produced by beta- amyloid protein (a protein overproduced in Alzheimer’s brains)  http://youtu.be/kfAGDFSWlAc

9. Potential therapeutic targets of huperzine A for Alzheimer’s disease and vascular dementia Abstract: Huperzine A (HupA), a novel Lycopodium alkaloid isolated from Chinese folk medicine Huperzia serrata (Qian Ceng Ta), is a potent, selective and well-tolerated inhibitor of acetyl-cholinesterase (AChE). It has been proven to significantly improve the learning and memory impairment in Alzheimer’s disease (AD) and vascular dementia (VaD) patients in China. Interestingly, our recent data indicate that HupA also possesses other protective functions. This paper will give an overview on the protective effects of HupA, which includes regulating-amyloid precursor protein (APP) metabolism, protecting against A -mediated oxidative stress, apoptosis and mitochondrial dysfunction, as well as anti-inflammation. The multiple neuroprotective effects of HupA might yield additional beneficial effects in AD and VaD therapy.

10. A phase II trial of huperzine A in mild to moderate Alzheimer disease ABSTRACT Objective: Huperzine A is a natural cholinesterase inhibitor derived from the Chinese herb Huperzia serrata that may compare favorably in symptomatic efficacy to cholinesterase inhibitors currently in use for Alzheimer disease (AD). Methods: We assessed the safety, tolerability, and efficacy of huperzine A in mild to moderate AD in a multicenter trial in which 210 individuals were randomized to receive placebo (n= 70) Or huperzine A (200 microg BID [n=70] or 400 microg BID [n= 70] for at least 16 weeks, with 177 subjects completing the treatment phase. The primary analysis assessed the cognitive effects of huperzine A 200 mcg BID (change in Alzheimer’s Disease Assessment Scale–cognitive subscale [ADAS-Cog] at week 16 at 200 mcg BID compared to placebo). Secondary analyses assessed the effect of huperzine A 400 mcg BID, as well as effect on other outcomes including Mini-Mental State Examination, Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change scale, Alzheimer’s Disease Cooperative Study Activities of Daily Living scale, and Neuropsychiatric Inventory (NPI). Results: Huperzine A 200 mcg BID did not influence change in ADAS-Cog at 16 weeks. In secondary analyses, huperzine A 400 mcg BID showed a 2.27-point improvement in ADAS-Cog at 11 weeks vs 0.29-point decline in the placebo group (p 0.001), and a 1.92-point improvement vs 0.34-point improvement in the placebo arm (p 0.07) at week 16. Changes in clinical global impression of change, NPI, and activities of daily living were not significant at either dose. Conclusion: The primary efficacy analysis did not show cognitive benefit with huperzine A 200 mcg BID.

11.  Claims state that Huperzine A help support memory retention and prevent breakdown of key neurotransmitters in the brain.  Some studies show promising results in the use of Huperzine A in the slowing of progression of Dementia and Alzheimer’s Disease.  Further studies are still needed to prove long term effects.

12.  Possibility of cholinergic syndrome when paired with other AChE inhibitors.  When taken may cause upset stomach, indigestion, nausea, vomiting, sweating, twitching, slurred speech, bradycardia and restlessness.  Long term effects have not been studied, so prolonged use is not recommended.

13.  1. Would you choose Huperzine A over the prescribed AChE inhibitors? If so why/why not?  2. Why is blocking the AChE important in the cognitive function in patients with AD?  3. What is something you would change in either study to make it a more effective study?