Transcript of Tracie Wymer Julie Franks Shirin Malek Inflammatory Diseases.
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- Tracie Wymer Julie Franks Shirin Malek Inflammatory
Diseases
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- 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
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- Alkaloid compound By mouth: doses of 50-200 mcg twice daily
depending on the brand
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- 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.
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- Alzheimers 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
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- 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
Alzheimers brains) http://youtu.be/kfAGDFSWlAc
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- Potential therapeutic targets of huperzine A for Alzheimers
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
signicantly improve the learning and memory impairment in
Alzheimers 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-inammation. The multiple
neuroprotective effects of HupA might yield additional benecial
effects in AD and VaD therapy.
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- 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 Alzheimers Disease Assessment Scalecognitive 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, Alzheimers Disease Cooperative StudyClinical Global
Impression of Change scale, Alzheimers 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.
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- 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 Alzheimers Disease. Further
studies are still needed to prove long term effects.
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- 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.
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- 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?