ApoE4.Info

CarrieS wrote:

Plumster wrote:

I’m quite certain I have that crap in my brain and don’t know what to do about it aside from eating A LOT of broccoli. Any ideas?

I was going to say liposomal gluthathione, possibly, but it looks like inhaling glutathione is preferred. I've never tried it, not even sure where to get it:
https://www.ncbi.nlm.nih.gov/pubmed/18517105

And more fruits and vegetables:
https://www.hindawi.com/journals/omcl/2014/671539/

Dr. Ben Lynch has a liposomal glutathione drops here. He has this article about Sensitivity to Smells that you may be able to glean information from too.

I have been doing some research on glutathione as I'm adding to my list of supplements for a variety of reasons. Came across this by Chris Masterjohn, someone I listen to quite a bit (and he's mentioned on here by some): https://chrismasterjohnphd.com/blog/201 ... pplements/
He goes through the pros/cons of types, what may or may not work best, ect.

Plumster wrote:

I have been doing some research on glutathione as I'm adding to my list of supplements for a variety of reasons. Came across this by Chris Masterjohn, someone I listen to quite a bit (and he's mentioned on here by some): https://chrismasterjohnphd.com/blog/201 ... pplements/
He goes through the pros/cons of types, what may or may not work best, ect.

I would also just add here that not everyone tolerates glutathione supplementation genetically. I get a headache when I take liposomal glutathione, which is a sure sign that I should not be taking it. I'm taking NAC currently instead.

Abstract

Evidence suggests exposure to particulate matter with aerodynamic diameter <2.5 μm (PM2.5) may increase the risk for Alzheimer’s disease and related dementias. Whether PM2.5 alters brain structure and accelerates the preclinical neuropsychological processes remains unknown. Early decline of episodic memory is detectable in preclinical Alzheimer’s disease. Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer’s disease associated with exposure. Participants included older females (n = 998; aged 73–87) enrolled in both the Women’s Health Initiative Study of Cognitive Aging and the Women’s Health Initiative Memory Study of Magnetic Resonance Imaging, with annual (1999–2010) episodic memory assessment by the California Verbal Learning Test, including measures of immediate free recall/new learning (List A Trials 1–3; List B) and delayed free recall (short- and long-delay), and up to two brain scans (MRI-1: 2005–06; MRI-2: 2009–10). Subjects were assigned Alzheimer’s disease pattern similarity scores (a brain-MRI measured neuroanatomical risk for Alzheimer’s disease), developed by supervised machine learning and validated with data from the Alzheimer’s Disease Neuroimaging Initiative. Based on residential histories and environmental data on air monitoring and simulated atmospheric chemistry, we used a spatiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1. In multilevel structural equation models, PM2.5 was associated with greater declines in immediate recall and new learning, but no association was found with decline in delayed-recall or composite scores. For each interquartile increment (2.81 μg/m3) of PM2.5, the annual decline rate was significantly accelerated by 19.3% [95% confidence interval (CI) = 1.9% to 36.2%] for Trials 1–3 and 14.8% (4.4% to 24.9%) for List B performance, adjusting for multiple potential confounders. Long-term PM2.5 exposure was associated with increased Alzheimer’s disease pattern similarity scores, which accounted for 22.6% (95% CI: 1% to 68.9%) and 10.7% (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1–3 and List B, respectively. The observed associations remained after excluding incident cases of dementia and stroke during the follow-up, or further adjusting for small-vessel ischaemic disease volumes. Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer’s disease risk, independent of cerebrovascular damage. [Emphases added]

Fiver wrote:Yes. The evidence is strong and accumulating. Not just for AD but also other dementias and Parkinson's disease, not to mention the rock solid evidence it contributes to CVD. Unfortunately, the nation isn't doing much about it. In fact, PM2.5 pollution is up in recent years, after declining for almost a decade in most areas. My area is hard-hit by PM2.5, mostly from trucking and warehouses. I doubt that any amount of evidence would sway local politicians, since there is much $$ at stake.