if you are worried about
Hupoerzine A you could stop and cycle it with phosphatidylserine (PS) and/or Acetyl-L-carnitine
Its Antiaging Effects
ong-term use of phosphatidylserine (PS) in aged rats has been found to preserve cholinergic neurons.1 This is good news for aging humans. The proper function of these brain cells is instrumental to proper memory. In fact, there was no difference in cholinergic neuron count when compared to rats less than 1/6 their age, whereas the number of these neurons fell by 20% in age-matched rats not receiving PS.
Scientists have found as well that chronic PS use improves acetylcholine (ACh) release in aged rats.2
ACh is a neurotransmitter known to be essential in memory function. It is the means by which messages are transmitted in the cholinergic system, and it enhances the activity of all neurotransmission activity in the brain. ACh may be thought of as the electrolyte of the brain.
PS increases ACh release by increasing the availability of the nutrient choline for ACh synthesis. It also appears to restore acetylcholine release in aging rats by maintaining an adequate acetylcholine supply.3 [See new recommended intakes for choline in Durk Pearson & Sandy Shaw Life Extension News - Issue #5.]
When 149 elderly humans with age-associated memory impairment were given PS for 12 weeks, their ability to perform quality of life learning and memory tasks improved.4 Improvement was greatest for those who were more impaired than their age peers. The results indicate that PS helps restore proper memory function later in life.
Acetyl-L-carnitine enhances acetylcholine release
Acetyl-L-carnitine enhances acetylcholine release in the striatum and hippocampus of awake freely moving rats.
Imperato A1, Ramacci MT, Angelucci L.
The effect of acetyl-L-carnitine (ALC) on the spontaneous release of acetylcholine (ACh) in the striatum and hippocampus of freely moving rats was investigated using brain microdialysis coupled with HPLC-electrochemical detection. Systemic administration of ALC, in a dose-dependent manner, stimulated ACh release in both areas, while the D-enantiomer was substantially ineffective. The effect of ALC was strongly Ca2+ dependent and tetrodotoxin (TTX) sensitive. These features of an exocytotic and impulse flow-dependent mechanism suggest that the increase in ACh release is the result of ALC activation of a physiological mechanism in cholinergic neurons.