Cholesterol - Making the Synapse


A few years ago Frank Pfrieger reported to the world that he had found the synaptogenic chemical that had eluded researchers for years.

It was cholesterol, the much maligned substance that for 40 years had been considered public health enemy number one. Of course this misconception was nonsense but it ruled our minds and medical school teaching for several generations of new doctors.

Now physicians are finally awakening to the new reality that cholesterol is not the cause of atherosclerosis but the new paradigm is all but indigestible. Four decades of false premise is not easy to overcome. This bowing to a false God has been not only a waste of time but the emotional burden of having been proven wrong for all these years is extraordinarily difficult for doctors now to accept.

Many still cling desperately to bits and pieces of the collapsing façade of cholesterol causation as if seeking to somehow escape the truth, but they cannot escape, only delay confrontation with frustrated and increasingly skeptical patients.

Since Pfrieger's seminal work, other research scientists have tried to identify the specific means by which cholesterol performs it miracle in the brain. Much work has been done. Recognizing that glial cells, known also as astrocytes, seemed to be the source of this synapse promoting factor, scientists soon identified from mass spectrometry and micro sequencing that in this glial cell medium was a cholesterol carrier known as Apo lipoprotein (ApoE).

They found that ApoE receptors were particularly abundant on neurons but only in the presence of additional cholesterol, itself, would the neurons be enticed to truly work their magic on synapse formation. Apo (E) by itself provoked only modest synaptic results, whereas the addition of extra cholesterol clearly was required. Even though they still are trying the identify the exact step in this sequence of events, the one thing the researchers agree upon was that without an abundant supply of cholesterol, synaptic formation and function can not occur.

Obviously, anything tending to limit cholesterol availability such as powerful statin drugs must inevitably have an effect on neuronal synaptic formation and brain function. Since synapse formation is mandatory for cognition, not only is cognitive dysfunction likely with statin use, it is inevitable.

I sincerely doubt drug companies would have developed statins for cholesterol inhibition had they known of the importance of cholesterol to cognition, yet this information was published for all to see in 2003 and statin sales are currently booming. Not even a hint of a black box warning to this effect. Yet thousands of amnesias and other cognitive symptoms are residing in FDA's Medwatch, not acted upon because it would appear, no one is looking at them.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor


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