Ben A. Barres and Stephen J Smith. Science, November, 2001, Vol 294, pp1296-7.
"The smooth operation of the nervous system depends on rapid commmunication between nerve cells at meeting areas called syapses. Although synapses were first identified 100 years ago, their fomation, a process called synaptogenesis, has remained something of a mystery....two intriguing but unanticipated conclusions about synaptogenesis have been reached. The first is that neurons by themselves form few synapses unless they have help from other nerve cells called glial cells(1-3). The second reported by Mauch, et. al..., is that the synapse-promoting signal released by glial cells is CHOLESTEROL(emphasis mine)...

...Neurons in culture form few synapses unless glial cells called astrocytes are present. Astrocytes increase synapse number by secreting cholesterol bound to large lipoprotein particles containing apolipoprotein E (apoE).

These particles are internalized by neurons, leading to increased cholesterol within neuronal membranes . It is possible that apoE also activates yet to be identified signaling pathways within the neurons . These changes stimulate an increase in the number and efficacy of synapses."

Refs noted in above quote:
1. FW Pfrieger. BS Barres, Science 277. 1684 (1997)
2. EM Ullian., S Sapperstein, et al Science 291, 65 (2001)
3. K. Nagler, D. Mauch, j Physiol533. 665 (2001)
4. DH Mauch, et al Science 294. 1354 (2001)

[as an aside --apoE IS the SAME lipoprotein that researchers "target" by statin use in patients with alzheimer's--statins decrease apoE, which many researchers "theorized" was responsible for amyloid aggregation found in Alzheimer's--and because individuals with APOE-4 gene variations have been shown more susceptible to developing Alzheimer's in a couple of studies...what if their theory is incorrect??]

It may or may not be important that the lipid that constitutes the largest percentage of all fats found in the SUBSTANTIA NIGRA is "dolichol" and dolichol production is directly dependent upon the mavelonate pathway--the same pathway that is totally blocked by all statins. does this fact have clinical relevance--who knows--no one has asked the question. it is just assumed that it must be okay..or hoped that it is in fact not an issue. or by not addressing it, it is in fact a non issue....