Welcome, Eric!Eric wrote:I wonder if certain statins could be helpful is resisting dementia for those of us who have two APOE e4 genes. I ask this based on a paper which reanylzed the data on tests of statins that did not work in general to slow Alzheimer’s. The statistics on us homozygotes were actually pretty positive. I think it can be looked up at the following url. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5316146/
In the abstract of that paper is::
Re-analysis of AD patient-level data from failed clinical trials suggested by trend that use of simvastatin may slow the progression of cognitive decline, and to a greater extent in ApoE4 homozygotes.
The charts in that study are stunning. It seems to virtually prevent decline, though it seems there are only about twenty people that fit into this re-analysis. Still...
I personally had my doctor prescribe me 80 milligrams of atorvastatin because I was taking 20 milligrams without any problem. I think this is equivalent to simvastatin because it is one of the so-called lipophilic statins that probably goes through the blood brain barrier. My LDL went way down, to about a third of what it was with no statin, which I think is probably protective against vascular problems, which is also good.
Anyway, I wonder what others might think of my choice.
Fiver wrote:The debate about statins is a long one. The best course of action almost certainly depends on our own situations.
I've been on low dose statins, of various sorts, for 3-4 years now. The research convinced me that overall the benefits outweighed the side effects for me. I like that they have an anti-inflammatory effect. They also prevented the usual spike in "bad" cholesterols and TGs when I began a ketogenic diet and was eating lots of nuts and chocolate - yes, this felt a bit like cheating but it worked.
Hi Eric,Eric wrote: If you have any real research about dementia though, please send. I will read it for sure.
The role of Apolipoprotein E epsilon4 in the association between psychosocial working conditions and dementia...it has been shown that education, job complexity, leisure activities, and social network may attenuate the genetic risk of dementia due to APOE ɛ4 , possibly by enhancing cognitive reserve and reducing stress levels. Similarly, in this study, active jobs appeared to nullify the detrimental effect of genetic predisposition, as the risk of dementia among APOE ɛ4 carriers with active jobs was similar to that of the non-APOE ɛ4 carriers with active jobs.
Results: Highest efficacy was observed in APOE4/4 homozygotes receiving 150 mg BID of tramiprosate, showing statistically significant effects on ADAS-cog and positive trends on CDR-SB (respectively, 40-66% and 25-45% benefit compared to placebo). APOE4 heterozygotes showed intermediate efficacy, and non-carriers showed no benefit. In 426 patients with MRI scans, no cases of treatment-emergent vasogenic edema were observed. In the three subgroups, the most common adverse events were nausea, vomiting, and decreased weight.
Conclusions: The “APOE4 Gene-Dose effect” is likely explained by the high prevalence of amyloid pathology in symptomatic APOE4 carriers. In APOE4/4 Alzheimer’s disease patients, the high dose of tramiprosate showed favorable safety and clinically meaningful efficacy in addition to standard of care.
The effect of ApoE ε 4 on clinical and structural MRI markers in prodromal Alzheimer’s diseaseIn 2018, the National Institute on Aging and Alzheimer’s Association (NIA-AA) proposed a new research framework focusing on diagnoses of AD with biomarkers for living persons (17). The scheme [which is labeled AT (N)] is based on grouping biomarkers into 3 categories: β amyloid deposition (A), pathologic tau (T), and neurodegeneration (N) (17). ...ApoE ε 4 (+) prodromal AD participants had lower levels of CSF Aβ 1-42, higher levels of t-Tau, more memory and global cognitive impairment, and faster decline of global cognition, compared to ApoE ε 4 (−) prodromal AD. ApoE ε 4 (+) prodromal AD participants had a thinner cortical thickness of bilateral entorhinal, smaller subcortical volume of the left amygdala, bilateral hippocampus, and left ventral diencephalon (DC) relative to ApoE ε 4 (−) prodromal AD. Furthermore, the cortical thickness average of bilateral entorhinal was highly correlated with memory and global cognition.
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