"Frank Pfrieger announced to the world in 2001 the importance of cholesterol to the process of memory. So critical is this relationship that our brain's glial cells have been tasked with the role of synthesizing cholesterol on demand to meet the needs for memory synapse formation and function.
This was far too critical a role to depend upon normal blood levels of cholesterol, for the lipoprotein bound cholesterol molecule presents too large a molecular structure to pass the blood brain barrier. We have evolved as a species totally dependant upon our glial cell source of cholesterol for memory.
The effects of statins on this glial cell function is quite predictable - inhibition! This results in transient global amnesia episodes in some, confusion, disorientation and increased forgetfulness in others, increased senility in those already afflicted and permanent loss of short term memory in others.
This is the underlying relationship of cholesterol to memory function in all of us. This dependency upon cholesterol for cognition is our heritage. The purpose of the Whittehall II study was to examine the relationship between fasting serum lipids and short-term verbal memory in middle-aged adults.
The authors concluded that over a 5-year follow-up period, HDL-C measurements (this is the common so-called good cholesterol) were associated with poor memory and decline in memory, respectively. No other lipid that was tested was associated with memory changes.
Regardless of the media hoopla, the cholesterol lowering effect of all statins can only be detrimental to cognitive function. Any possible benefit of a statin must arise from the anti-inflammatory effect of statins, a process discovered only 5 years ago and thoroughly explained by Ora Shovman (2).
Because of this effect statins are sometimes used on such inflammatory diseases as lupus erythematosus and rheumatoid arthritis and even in organ transplant therapy. I suspect there is an inflammatory component to Alzheimers that is favorably influenced by statins yet the simultaneous inevitable reduction in cholesterol can only be detrimental to cognitive function. This presents an obvious therapeutic checkmate concerning the use of statins for dementia.
The authors explain that there is some evidence suggesting that dementia itself modifies lipid levels, leading to low total-cholesterol or low-density lipoprotein cholesterol (LDL-C) levels among those with dementia and predict that examination of the effect of lipids on cognition in the elderly is likely to yield spurious results. They add that associations between mid-life lipid levels and late-life dementia in their study were robust.