Anonymoose wrote:I've been reading up on cholesterol to try to decide my next step. According to this study ( http://www.jneuroinflammation.com/conte ... -8-127.pdf ), high LDL is associated with greater brain atrophy/loss of mass. Higher HDL and lower triglycerides is associated with fewer enhancing lesions. Which cholesterol level was low? (I'm waiting for cholesterol levels too).
Abstract wrote:Although an increased leukocyte and platelet adhesion is observed in cerebral venules of mice with either hypertension (HTN) or hypercholesterolemia (HCh), it remains unclear whether the combination of HTN and HCh exerts a comparable effect on leukocyte and platelet recruitment in the cerebral microvasculature. Thus, we examined whether HCh alters platelet and leukocyte adhesion, and blood–brain barrier (BBB) permeability, in cerebral venules in two models of murine HTN: DOCA salt-induced and angiotensin II (Ang II) induced. In both models, the mice were placed on either a normal or cholesterol-enriched diet. An enhanced recruitment of adherent leukocytes and platelets in cerebral venules was noted in both HTN models in the absence of HCh, but not in its presence. The Ang II-induced increase in BBB permeability was attenuated by HCh as well. Both total and high-density lipoprotein (HDL) cholesterol levels were elevated in the HCh mice. The HTN-induced increase in leukocyte and platelet adhesion was attenuated in apolipoprotein A-I transgenic mice (ApoA1-Tg) and blunted in wild-type mice treated with the ApoA1 mimetic peptide, 4F. Our findings indicate that mild HCh significantly blunts the cerebral microvascular responses to HTN and that HDL may have a role in mediating this beneficial effect of HCh.
Conclusion wrote:In conclusion, the results of this study indicate that mild HCh significantly blunts the recruitment of leukocytes and platelets in the cerebral microvasculature in both low and high Ang II models of HTN. Our findings are also consistent with a role for HDL and ApoA1 as mediators of this antiinflammatory and antithrombogenic effect of a cholesterol-enriched diet. These observations suggest that HDL and ApoA1 may be effective therapeutic targets for prevention of the systemic inflammatory response that accompanies HTN. Whether our results bear on the responses of intracranial arteries to the combination of HTN and HCh remains unclear. The beneficial effects of ApoA1 mimetic treatment on the cerebral microcirculation suggest that elevations in HDL or administration of the ApoA1 mimetic may also afford some level of protection against any impairment of endothelial function in intracranial arteries that result from chronic arterial HTN. However, additional work is needed to directly address this interesting possibility.
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