Tuesday, December 21, 2010

Alzheimer's and HDL

There are a number of December papers I've been wanting to blog about, but other things came up along the way.  But here I have a moment before the children come home, and the house is quiet except for the cats... I ought to be wrapping presents... but here is a new Alzheimer's paper to add more confusion to the cholesterol and Alzheimer's information.  Overall, the data have suggested that high cholesterol in midlife and low cholesterol in late life both increase risk for the development of Alzheimer's in late life. 

As usual the lipid hypothesis holds sway, and when one reads the analysis in the literature, one gets the idea that the high cholesterol in midlife is likely a causative factor, whereas low cholesterol in late life is "part of the disease process."  (For example, Grandfather must be eating less because he is getting demented, so his cholesterol drops.  For years prior to severe symptoms that might legitimately lead to eating less.)  Of course I'm of the opinion that cholesterol is good for the brain.  But not too many people listen to me.  Or else the  The Primal Blueprint Cookbook: Primal, Low Carb, Paleo, Grain-Free, Dairy-Free and Gluten-Free would be in the top 5 bestselling cookbooks rather than number 5 on the Physician's For Responsible Medicine's Worst Cookbooks of the Year. (Hah they even have the huevos to remark upon the silly "low carb animal" vs. "low carb vegetable" study that came out earlier this year as evidence for avoiding Mark's book!!)  I think I might pick up a few more books on that list of the worst five, frankly.  They look as if they contain many delicious recipes.   

Okay, back to the paper.  Did you know that more than 50% of the adult US population has high cholesterol?  And 1% of people ages 60-69 will develop Alzheimer's, increasing to more than 60% of those over 95.  "There is evidence that cholesterol alters the degredation of the amyloid precursor protein" (supposedly bad) but "cholesterol depletion induces [Alzheimer's Disease]-type injuries in cultured hippocampal slices" (now that sounds quite bad.)  Overall, the observational studies linking dyslipidemias to Alzheimer's have been inconsistent (with the typical take from the literature what I discussed in the 2nd paragraph above).  

Well, high LDL and low HDL have been linked in the past to vascular dementia.  Vascular dementia is kind of the brain version of heart disease.  Arteries get clogged up with plaque (different plaque, actually, than amyloid plaque, things get blocked, mini-strokes occur, and someone gets gradually demented as the amount of damage builds up. Anyhoo, Alzheimer's is a bit different - neuronal amyloid plaque builds up, then you get inflammation and tau tangles, and neuron damage and death.

The authors of this study wanted to examine a cohort of people after the start of widespread use of lipid-lowering agents (primarily statins) in the 1990s.  So these folks in "Northern Manhattan" were recruited from the Medicare roles in 1999-2001, baseline measures of general health and cognitive function were gathered, and they were followed up every 18 months or so.  Out of 1130 individuals who completed the study, 101 were diagnosed with AD, 89 diagnosed as having probable AD, and 12 as possible AD (while Alzheimer's Dementia can only be definitively diagnosed via autopsy, there is a characteristic style of progression of memory loss that makes the performance on certain cognitive tests a decent way of diagnosing the disease).

The mean age of onset of the disease was about 83.  Higher HDL (especially over 56 mg/dl) was protective after adjusting for all sorts of things, including age, ApoE4 status, sex, education, ethnic group, and even vascular risk factors and lipid-lowering treatment.  Interestingly, higher total cholesterol levels and higher LDL cholesterol levels were also protective through all the adjustments except the last two, though became nonsignificant when lipid-lowering treatment and vascular risk factors were adjusted for. (In this cohort, high insulin levels were a strong risk factor also).

The authors put forth the "HDL as garbage trucks" hypothesis of HDL cleaning the cholesterol out, and they postulate the following: "High-density lipoprotein cholesterol might also be linked with small-vessel disease by ...interaction with with APOE and heparan sulfate proteoglycans in the subendothelian space of cerebral microvessels.  Thus, a low HDL-C level could precipitate AD through a cerebralvascular pathway."  (Or how about this theory, which is my own little edit - high HDL-c is associated with low amounts of inflammation and that is the secret to a healthy brain). And more discussion in the paper is about how the study of lipids and Alzheimer's has been confusing all along, and certainly low HDL is associated with stroke, so maybe also some linked pathology is responsible in AD... and previous cohorts with higher total cholesterol in midlife blah blah...  this paper twists and turns about so many times I get confused.

Don't be confused.  Let go of the lipid hypothesis.  Think inflammation.  It's the immune system, not the liver, that is trying to kill us.  Then everything becomes clear, and things start making sense again.  Peace.

17 comments:

  1. I mean to get to a blog post on your excellent Alzheimer's series but here's a note:

    High lipids in midlife reflect metabolic syndrome, which implies hyperglycemia, which promotes bacterial infections. These would initially enter in the gut and vessels and might take decades to spread to the brain.

    Cholesterol is important for immune function and low cholesterol is a huge risk factor for infectious disease. So low cholesterol might lead to progression of any established brain infections.

    This would help reconcile the seemingly paradoxical observations.

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  2. I like this post Emily.

    The idea that HDL is in part a marker of inflammation (correlating negatively with it) makes sense to me. And maybe this is a very strong correlation.

    I still think it is also a marker of one's diet (correlating positively with saturated fat), and probably plays the "garbage collector" role as well.

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  3. Two factors correlated with low incidence of Alzheimer's in this study:

    High HDL
    Low insulin levels:

    How do you achieve both factors-restrict your carbs.

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  4. part 1




    I'd like to put a strange twist on amyloid plagques found in people with Alzheimer's.

    I saw Emily had mentioned these amyloid cells in a prior blog, as with anything new to me, I google it, and came across several articles that promote amyloid plaques CAUSE Alzheimer's.

    After reading that these star shaped cells are - garbage cleanup - as the key word in the article above triggered ? I got to thinking, MAYBE the concentration of amyloid plaques isn't CAUSAL to Alzheimer's BUT... MAYBE it's a RESPONSE to something else, such that the body is promoting more amyloid cells to go clean UP - and that in fact ? They are actually helping, and something else is the cause to which they are merely the response TO. Uh oh, back to 8th grade English, I just ended a sentence with a prepsition ! augh!

    Anyway, seeing this HDL being suspect as causal factor in AHD? I thought I'd share that insight, as it is fleeting !

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  5. Learning about Amyloid Plaques recently ?

    I got to thinking: Basic on THIS article:

    http://www.chiff.com/articles/alzheimer-amyloid-plaques.htm

    Titled: Amyloid Plaques in Alzheimer's Disease
    Linked to Malfunction of Normal Memory Genes


    As I tried to post earlier, maybe the Plagues are a response to something ELSE - but no room for any of that in the 4096 bytes - so I'll just share this one:

    I got to thinking of course "How to dissolve amyliid plaques" and put that into google.

    Which got me this:

    http://scienceblog.com/1216/pain-killers-may-dissolve-alzheimers-disease-plaques/

    title implicit in link.

    Interesting to say the least.

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  6. Regarding my theory that Amyloid Plaques are a RESULT of something else ?

    I'm willing to throw that out the window and say- hey - it could be WAY off, BUT...

    Yet another neat article on bottom line, how to melt away those plaques.


    http://newsletter.vitalchoice.com/e_article001362829.cfm?x=bfcvnPk,b7b1jv7h,w

    Fermenting Soybean enzyme melts the plaques away it seems.

    Indeed, I'd LOVE to see an Alzheimers resource site, as a senior software engineer and web developer ? I often say - okay, I'll set itup in a directory off of one of my hair brained projects -

    But this fermented soy ? seems like it would be a GOOD Dietary regimen for anyone with AHD - UNLESS, as I said earlier, those plaques are a defensive measure. Since Amyloid cells are cleanup cells.

    I often notice this with my teeth, I NEVER brush them, and I maintain plaque, BUT, if and when I DO brush them ? BAM, instant toothaches for days, I now look at it as if somehow on one hand the plaque is harboring bacteria that consumes sugars and causes the cavities BUT it also seems to protect by a layer against other things getting into those cavities.

    I'm wondering if plaque is a defense mechanism.

    Either way - I'm adding that soy reference to my list of AHD remedies... that neuronal regrowth news weeks ago I think was most promising.

    Who'd have thought, neurochemistry for 50 years up until 2 weeks ago was dead wrong that neuronal cells don't regenerate, turns out we've have the neuronal stem cells all along, just needed to turn on production.

    Probably won't be in any western medical textbooks for 15 years.

    The physicists at CERN created HTML to make text TRULY dynamic, and yet ? here we are in 2010 ? and we BARELY have Web 2.0 implemented, and for the most part ? don't have ANY dynamically derived textbooks. Just amazing, I see the tablet PC's available in 2000 have FINALLY made a successful marketing run ! aubgh!

    TEN YEARS LATER.

    Gotta think for yourselves people !

    No one else out there probably has your health in interest, at least pro bono.

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  7. Last year, she ran across a report of Axona's clinical trials, well before it hit the market. Not wanting to wait, she began feeding her husband large doses of virgin, nonhydrogenated coconut oil, available at Wal-Mart for less than $7 a quart.

    Coconut oil contains a mixture of saturated fats. The liver converts some into ketones. Others float around in the bloodstream, which is why cardiologists usually discourage its use.

    The effect on Steve Newport was immediate.

    "He said it was like someone had turned on a lightbulb,'' Mary Newport says. "He was alert, smiling, joking. He was Steve again. He was back.''

    http://www.tampabay.com/news/health/research/article1024137.ece

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  8. I was just closing my windows in browers? and I came across that article on pain killers being used to break down amyloid plaques ?

    I just HAD To share this insight that just occurred as I read this.

    I once thought I had cancer, so I researched means and ways for blocking tumor angiogenesis, one doctor at Harvard Medical School, pediatrics iirc, put forth that NSAID's Cox-2 (over 20 years ago iirc his thesis, might hav eeven been the 1970's) is responsible for blocking tumor angiogenesis, and I recall a Dr. Brewer at Univ. of Michigan who realized a relationship between copper and zinc, that is, increasing ONE WILL decrease the other, and he further realized loading up on zinc, and decreasing copper would ALSO bring tumor anti-angiogensis, I further learned of many anti-oxidants that can lead to apoptosis of the tumor such as ellagitannins and - well AAAAAAYYNWAY, I JUST REALIZED SOMETHING HERE.

    On learning this about Cox-2 and NSAID's - I looked up what plants are highest. I learned Ginger is highest of all plants, to which ? Anything you'd take ibuprofen for ? I'd research this to validate it yourself (I know I'm right here ? but you should ALWAYS check anything you read, in my learning process/ae online, I encounter MORE misinformation, some disinformation than good information when it comes to plants, I try to stick to Chinese apothecary sciences as I like to call it, and Ayurvedic for herbs) AAYYYYYNYWAY....

    I DO RECALL -

    Guess what is NSAID #2 in nature ? well- of known plants ?

    Come on - GUESS

    What is ALSO the ONLY ingredient included in MIT's as well as THE BIG news in neuronal regrowth in November in the world of science ?

    Turmeric is #2 on my list of the most powreful NSAID's in nature.

    now, what HIT me here as I was closing the browser on this article:

    http://scienceblog.com/1216/pain-killers-may-dissolve-alzheimers-disease-plaques/
    A quote from the article that struck me:

    "He discovered that common over-the-counter pain medications — known as non-steroidal anti-inflammatory drugs — bind to amyloid plaques, and may help dissolve existing plaques and prevent the formation of new ones. "

    Ever since I read Dr. Deans blog that mentioned Amyloid cells - to which I had never heard of, I learned that Alzheimers patients hvae REAL high levels of Amyloid plaques in their brains.

    NOW NOW - JUST saying, MAYBE the reason Turmeric- the SOURCE for Curcumin (Curcumin IS the name for the KEY ingredient turmeric (curcuminoids)? is included in the neuronal regrowth criteria (there were 4 mentioned in the study I read (MIT included sugar cane exrtact, a 5th), low caloric intake, exercise, curcumin and choline) that triggered the neuronal regrowth from neuronal stem cells WE HAVE ALREADY - ready to go.

    So, putting 1 plus 1 here, I DO WONDER if all this news about even 1 teaspoon of turmeric PER YEAR helping to prevent alzheimers ? ALSO, just google Turmeric and Alzheimer's - the connection is shown EVERYWHERE, I am just saying, I wonder IF it's not the anti-oxidant properties of curcuminoids ? BUT - REALLY, BECAUSE Curcumin is an NSAID - or ? Hey - I always forget about option #3- BOTH, maybe it's a DOUBLE PUNCH, BOMNUS anti-oxidant that works in this region of the brain AND the NSAID PLAQUE DISSOLVING EFFECT of Turmeric.

    If anything, sounds like Turmeric is a MUST HAVE in any diet, come on, neuronal regrwoth ? Who'd want to pass that up... PLUS it's HIPPOCAMPAL neuronal regrowth- gee, memory center anyone ? I bought a Curcumin EXTRACT from a respected manufacturer two months ago, when I had a few bucks, I do say, MIGHT NOT BE A BAD IDEA people - to explore that. I won't plug brand or site where I get my products, but the site I use I find has the best deals and best shipping - if you see the initials VC, you're on the right track... Don't want a genuine message to get caught up as spam.

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  9. part 1 of 2 (was over 4096 characters):

    I know I have probably taken up too much real estate here in my stream of consciousness blogs I try to keep related to the subject, and I DO find these blogs by Dr. Emily Deans very intriguing - EVEN IF they are spawned by academic competitiveness !

    I just wanted to beat this drum one more time on realizing this morning paging through Amyloid Plaque being present with people with Alzheimers ?

    It REALLY looks like Curcumin has a double feature to helping Alzheimers. #1, this new news aboud NSAID's dissolving Amyloid plaques, and #2, this new OFF the CHARTS news in November (SEEMS it really happened in July 2010 iirc reading back) that we possess neuronal stem cells and we CAN trigger them, BEST PART ? They can rebuild cellular structure in the Hippocampus and the 4 fold criteria are RATHER simple - exercise, low caloric intake, CIRCUMIN, and CHOLINE (I've been taking Choline for fun and theory that it will help my memory [I'm 42] for easily 10 years now, plus the dreams are short of fantastic, especially if I take the Chinese Club Moss/Huperzine which inhibits Acetylcholinesterase, which itself helps AcH turn over, so you inhibit the inhibotor, was a Dr. Hobbs that got me into realizing AcH and dreams are connected, he published in the NYT Science times two decades ago that during REM the brain is just flooded with AcH with serotonin no where to be found practicaly [Hey hey Doctor Deans, ok ok maybe Serotonin and AcH are connected, at least one is high and the other low in REM]).

    I JUST wanted to share a solution I thought might be good, I am NOT suggesting anyone DO this, but it's something to consider. Maybe Dr. Deans is connected to more researchers that might explore this regimen.

    BEING that Choline + Curcumin + exercise + low caloric intake stimulate production and regeneration of the Hippocampus of neuronal cells ?

    AND that I JUST READ tonight that NSAID's AND go figure- a fermented Soy extract Tiawanese researchers discovered 'melt away' Amyloid fibers / Plaque ? from article:

    "Until now, no one had tested whether nattokinase can dissolve amyloid fibrils, which are resistant to normal protein-digesting enzymes (proteases) the body could otherwise use to help clear the brain of plaque.

    New lab results from Taiwan indicate that natto enzymes may degrade the amyloid protein fibrils that form part of the beta-amyloid plaque linked to Alzheimer’s disease (Hsu RL et al. 2009).
    "

    from http://newsletter.vitalchoice.com/e_article001362829.cfm?x=bfcvnPk,b7b1jv7h,w

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  10. better make that part 2 of 3 (and 1 of 3 on the last, STILL won't fit, says over 4096, I'm sure that's some database limitation)

    I suggest this for a model:

    You use nattokinase and NSAID's to dissolve the plaque, BUT- you ALSO run at the same time a regime to REBUILD - especially areas where the plaque was taking up, sadly ? I read the plaque does destroy parts of the hiipocampus, BUT hey - GOOD NEWS is - this neuronal regeneration IN the hippocampus, so, why not run nattokinase and NSAID's to dissolve the amyloid plaques at the same time - or maybe start before, a STRICT low caloric intake, plus STRICT MANDATED exercise PLUS strict choline intake, and of course, curcimin, I read an MIT team - of ALL things found sugar cane extract useful in the neuronal regrowth, sounds REAL SKETCHY to me, but MIT next to it ? hmm - I have a friend that just got his masters at MIT, and HE'S SKETCHY - hmm - heh heh, JK if you know who you are ! Well, FLAKY, but not sketchy. heh, I'm probably sketchy and flaky ! anyway, I wnated to put forth that idea, to run a program to dissolve the plaque AND utilize this NEW regrowth process discovered just months ago. Seems some memories might be gone ? NOT that I'm not a fan of Karl Pribram, I mean, he has the MOST hours logged of ANYONE during live brain surgery testing memory, and he settled that memory may not be 'residing' in any one place, so it's POSSIBLE that the plaques don't destroy 'memories' (that's getting into real bizarre waters there), but it's possible the amyloid plaques INHIBIT function of memory. Anyway Dr Deans, it might be somethign to seek a grant on, or check out, trials on dissolving the plaques AND attempts to regenerate hippocampal tissue/neurons.

    Seems like it beats the alternative, letting the amyloid plaques stick - hmm - oh what the heck, RIGHT WORD for once, around.

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  11. part 3 of 3 and I'm outta here !


    I can see Roche or Eli Lilly going "hey, can we get to work on some syntehtics and create a dual composite compound that does these both at the same time and cash in on this ? "

    I prefer to draw on cutting edge research, mix it in with existing research, then I always hit google for the key ingredients plus the word "plant" or "herb" and usually find a plant source that - well- my motivation is cost, as I never have any money ! lol

    The Turmeric is DOUBLE BONUS remember, NSAID PLUS it's got the one UNIQUE criteria listed in the 4 criteria for neuronal regeneration.

    Who knows, maybe DHA WITH Choline and Curcumin really help regrowth, I once read alcohol flushes away DHA in the brain, as DHA is a big component of grey matter atleast. How bizarre brain terminology often ends up sounding so rudimentary, like 'grey matter'. JUST saying, taking DHA is supposed to help restore those necessary fats to the brain, if one is seeking neuronal regrowth, and removing plaque ? Might bea good idea to go heavy on DHA to get extra fats the brain is made up of in there too ! DHA has it's place, I think I've settled on that, that it simply has A place, I used to think it was the end all be all. NO Meats either I'd think, because I read homecysteine can cause damange that is linked to AHD due to the neurotoxicity if one doens't have the methyl donors, which is why I started taking methyl B12 over B12, and Trimethylglicine, well, I have that on my wish list when I come up with $10 to spend along with that methyl based folate to which I figure - hey why NOT take that over folic acid considering 50% of people don't absord it too well, and some rare select few don't absorb it at all- gee, imagine who those people are, their whole lives, never getting folate, THAT would blow. Medical care should START with base genetics testing I think... find out who's got malfunctioning equipment to start, and compliment first before diagnosing anything. Just me hunch - but I'm not a doctor, I'm a software engineer ! and I've never NOT had bugs in my code, always SOME bug somewhere heh- This entire suggestion might be buggy, seems good to me, but someone in the field might say- throwing darts Tim, I say I INTUIT it makes a lot of sense and AHD is a losing battle so far. My concern would be maybe the RATE at which the amyloid plaque would dissolve, might be bad news to do it too fast before regrowth occurs.


    I STILL haven't finished my work this AM heh, got sidetracked with that Life with Louie show on the BBC, he goes to live with societally-pathogenic groups. I read in Japan, psychiatrists come to live with the patient for a few days sometimes. I think of ANY field, psychiatry is a GREAT field for this practice. For unless some doctor who sees a patient for maybe 1 hour a week or month for depress ? SEES that say Mrs. X is living in an apartment with ONE tiny 40 watt bulb ? and if they never ask about her lighting ? they may never KNOW that ANYONE living there would be depressed. I think ANY depression therapy should include questions about the indoor lighting.

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  12. Hi Tim - I appreciate your enthusiasm, but your comments are rather excessive in length and number. You really could consider your own blog as you have many interesting things to say.

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  13. part 1 of 2, ran out of space:

    Just wanted to share a relevant document to AHD I just found.

    And yes, it's regarding Curcumin- but in a NEW light, I already read Curcumin was one of the criteria for neuronal regrowth from research published this summer in July, and found it's way into mainstream press in November. I already learned that NSAID's are being shown from research in Taiwan (why do I geocode research sources ! heh) and Japan to 'melt away' Amyloid plaques. I knew from my own limited experience seeking NSAID's in herbs that ginger is #1, and that turmeric is a member of the same family as ginger, and go figure, turmeric is also an NSAID, so, chances are it is double bonus on NSAID use.

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  14. part 2 of 2

    Now, I myself was taking acetylcholinisterase inhibitors such as Chinese Sage (I get Planetary formula, I findally decided to share, but I'm not trying to plug their product), and I take Huperzine- derived from Chinese Club Moss (Many brands). I'm 42, and I figure I'll take them for memory, but I ALSO thought, and it seems a LOT of people have ALSO thought that - hey hey hey - maybe an acetylcholinesterase inhibitor would help with Alzheimer's, seems some pharmaceutical companies do too. By the way, I ALSO thought, due to the see-saw relationship between AcetylCholine and Dopamine ? that if you MAYBE decreased dopamine ? you'd elevate AcH - turns out someone else ALSO thought of that, and it didnt' work out, however I don't think anyone has tried a dopamine inhibitor WITH an acetylcholinesterase inhibitor WITH choline supplement, I DO wonder, you'd think THAT would elevate AcH - BUT ANYWAY... THAT Aside - which I didn't even think of until mid sentence there, I wanted to share THIS article which is NEW to me and might be of use to someone in a clinical setting -hint hint Dr. Deans ! :)

    http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0N-4TK476S-1&_user=10&_coverDate=02%2F28%2F2009&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1587194575&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3f1853355423f93b09b834bfe148922c&searchtype=a

    Go figure, Circumins have inhibitory acetylcholinesterase properties !!!!!!

    This means, TRIPLE BONUS then from Turmeric or - as I take when I can afford it- curcumin extract (I forget the brand, NOT plugging the site, but I finally decided to share, vitacost.com has competitive pricing, I am SURE there are better sites, I just use that site, plus a few Chinese herb suppliers but I have to say I'm a practitioner, but no illegalities as far as I know, all I get from them is Hu Zhang for it's resveratrol content, Huang Qi (astragalus for telomerase stimulation) and Huang Qin (Chinese scullcap for it's benzodiazipine activity but NON-ADDICTING, just to calm me down if I want to coast off to sleep better, AND it has - GO FIGURE - Chrysin, something I've been very interesed in lately).

    Well - that's all... Just the Curcuminoids have acetylcholinesterase inhibitory potential, was new to me tonight.

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  15. I'm going to throw a dart into the wind and suggest maybe Amyloid plaques are s defense mechanism against high homocysteine levels due to dropping methyl donors as we age.

    Why we lose methyl donors ? I don't know, but this is an intuitive hunch. I accidentally clicked on this Butter-Saturated fat blog here from Dr. Deans back in October. I'm even less understanding on fats - I saw a few sentences in the middle of the document stating that no amyloid fats from the gut is evidentiary.

    Like I said with my teeth, I never brush them, humans probably never brushed their teeth over tens of thousands of years, I have terrible teeth, and when I'd go to the Dentist ? just having them cleaned would leave me with toothaches, call me silly, but I intuit plaque is a defensive mechanism to somehow coat the teeth, I'm probably out to roost on that one, but I'm just thinking, maybe the amyloid plaques are a side effect of something else that is triggering their buildup, as if some protectionary mechanism/process from ? well -something neurotoxic, such as homocysteine.

    That's a TOTAL GRAB in the wind there.

    On that, I'm going back to work, and MAYBE just maybe I'll put together a base Alzheimer's information web page which is something I've been meaning to do, and let people add nodes for resources as they will to enhance a one stop shop for people looking into anything they can do to explore - well ANY chance at treatment of course, at their own risk.

    Myself ? My mother has AHD, but I'm not allowed to refer to it, bring it up, my father becomes hostile, just MENTIONING Chinese Sage (Salvia), I BARELY got out the words "I was reading that this Chinese sage may be helpful for Alz..." Decible level 90 - "You SELFISH SON OF A BTCH," gets up, screaming, runs off. It's simply not allowed to be talked about, and as far as my mother ? Lately she lasts maybe 5 seconds before the last question is asked fresh, brand new. He won't explore any diet change, sure they have a doctor, but that's hit or miss, I'm betting she's getting an acetylcholinesterase inhibitor through a pharmacological provision by the doctor. I can't tell her she has it, I can't even mention it with my father, so I figure ? Migth as well take everything I've learned and try to share it with someone who may be interested.

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  16. I just read a good article here as I was curious as to what CAUSES amyloid plaque buildup.

    SO FAR, it looks like this neprilysin (NEP) controls amyloid plaque levels. Some study at Brighams Young here:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941603/

    Shows -I'll quote the article:

    There is evidence that the Aβ-degrading protease neprilysin (NEP) is down-regulated in normal aging and LOAD. We asked whether a decrease in endogenous NEP levels can prolong the half-life of Aβ in vivo and promote development of the classic amyloid neuropathology of Alzheimer’s disease.

    ...

    NEP loss of function 1) elevated whole-brain and plasma levels of human Aβ40 and Aβ42, 2) prolonged the half-life of soluble Aβ in brain interstitial fluid of awake animals, 3) raised the concentration of Aβ dimers, 4) markedly increased hippocampal amyloid plaque burden, and 5) led to the development of amyloid angiopathy. A ~50% reduction in NEP levels, similar to that reported in some LOAD brains, was sufficient to increase amyloid neuropathology. These findings demonstrate an important role for proteolysis in determining the levels of Aβ and Aβ-associated neuropathology in vivo and support the hypothesis that primary defects in Aβ clearance can cause or contribute to LOAD pathogenesis.


    End paste:

    Looks to me like this NEP is UPSTREAM from amyloid plaque- and that means FIX NEP form decreasing ? and you fix Amyloid plaque buildup I'd think.

    So, off to learn about why NEP decreases. I bet it all ends up at losing methyl donors - LOL - jk.

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  17. Hi Emily. The comment above about fermented soy jogged my memory. There are studies showing that Vitamin K2 deficiency is linked to faulty sphingolipid metabolism in the brain.

    See Look after your brain. Cheers, Nige.

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