#Alzheimer’s_disease , #Obesity , #Zika –
The #Numbers , #$s , #Mystery , #KASH ; #Past #present & #future
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Mitochondrial respiratory chain defects- inherited disorders affecting approx 1 in 5000 people in the UK-pts w/mitochondrial disease show atrophy/severe neuronal cell loss that not assocd w/any extra- or intracellular accumulation of misfolded proteins $CWBR will Rx along w/ #AD https://twitter.com/fezziwig2008/status/936204510489432064
#Alzheimer’s Disease Protective Alzheimer’s Gene Variant Uncovered —>
Linkage, whole genome sequence, and biological data implicate variants in RAB10 in Alzheimer’s disease resilience
https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-017-0486-1 ThankYOU Dara! https://www.stockgumshoe.com/2017/11/notes-from-torrey-hills-capital-emerging-growth-conference-13-15-november-2017-san-diego-ca/comment-page-5/#comment-4962249
#Alzheimer’s Disease related – http://fortune.com/2017/12/01/human-longevity-dna-ceo-out/
#Zika – Army-Developed Zika Vaccine Induces Strong Immune Response In Three Phase 1 Studies https://scienmag.com/army-developed-zika-vaccine-induces-strong-immune-response-in-three-phase-1-studies/
#Alzheimer’s Disease related – How Loneliness Affects Our Health https://www.nytimes.com/2017/12/11/well/mind/how-loneliness-affects-our-health.html ht Dr. Ong rt ThankYOU! Best2ALL!
#Alzheimer’sDisease – Healthy mitochondria could stop Alzheimer’s
Date: December 6, 2017 Source: Ecole Polytechnique Fédérale de Lausanne
Summary:
Using a bioinformatics and experimental approach, scientists have found that rendering mitochondria resistant to damage can halt diseases caused by amyloid toxicity, such as Alzheimer’s disease. https://www.sciencedaily.com/releases/2017/12/171206132526.htm
#AD – Study Claims Urea Is Major Cause of #Dementia https://www.beingpatient.com/urea-dementia/ via @Being_Patient_
https://twitter.com/LEAD_Coalition/status/940918978129653760
#Huntingtonsdisease #Alzheimers #neuroscience @HDSA
What Happens When We Let Tech Care For Our Aging Parents? https://www.wired.com/story/digital-puppy-seniors-nursing-homes/?mbid=social_twitter_onsiteshare ht #ThankYOU Marianne! https://twitter.com/mtpoulsen/status/943378192705966080
#AlzheimersDisease #AD – Dr. KSS MD PhD Re: $PMN.v $ARFXF
My intent in commenting on ProMIS is not to make it look risible (I don’t question its sincerity in its approach and its belief in the authenticity of its work) but simply to caution investors and safeguard against capital losses.
I see several issues about its approach that are not necessarily problems unique to ProMIS:
(1) the amyloid hypothesis has serious deficits. Science cannot even answer why amyloid is elaborated, though we have made contentions in early commentaries about its origin.
(2) Two major theories of the ailment have gained considerable momentum: these would be the dampened synaptic transmission hypothesis and the RAGE receptor-driven neuroinflammation hypothesis. The Candida torulopsis hypothesis is strong but needs further testing by a clinical antimicrobial trial.
(3) people keep forgetting that monoclonal antibodies are possibly the worst reagents to be using to go after Alzheimers. They are being used as stoichiometric binding agents in pursuit of amyloid occupancy. But does this make sense? Satisfying establishment of the mere extent to which mAb’s, among the largest molecules the body sees, can cross the blood brain barrier is lacking. People also forget that IgG is complement-fixing, and thus evokes strong secondary inflammatory responses; ProMIS I admit is using an IgG4 that may have abated complement-inducing activities though I’d need to see data to be sure. But even if complement is not activated, there is the issue of Fc receptor binding after antigen engagement, and Fc receptors abound….on macrophages, other immune cells, even on platelets. Thereby CNS inflammation is further stoked. An anticalin would be vastly more ideal in pursuit of finding an anti-amyloid reagent, though I doubt any solution lies in the amyloid approach to things.
(4) no disease being pursued by biotech has a greater gulf between in vitro and in vivo investigative mechanisms; a cell culture model of AD that is genuinely relevant on all axes is impossible, and no definitive animal model exists. We cannot be invasive (ie, brain biopsies) in assessment of the histopathology, which radically alters itself upon death. A true solution may await further development of miniature CNS agglomerations ex vivo attained by 3-D bioprinting or by signalling of stem cells , along with tactics to replicate presence of an immune system.
(5) $CWBR has a mitochondrially elaborated peptide that reverses amyloid induced neurotoxicity and neuron paucity. The mechanism is only partly known but tends to undermine the amyloid hypothesis. Rather, I regard the best theory of AD is that it represents a local CNS diabetes with mitochondriopathy and failed constitutive mitochondrial peptide elaboration. Support of this model is amassing rapidly. I predict CohBar is on track to have a serious remedy for AD more so than any company in biotech, and this is based on non-privileged information albeit info the company has yet to present in a wide manner.
Above all else I certainly wish Michael Bigger good fortune in his investing pursuits and respect his considerable intelligence. I think it’s fair to assert here that Bigger may be aware of information that is not public and that being a sizable shareholder may have given him access, via an NDA, to data we cannot know that supported his decision to invest. And if so, I hope he wins and wins massively. His integrity, good attitude and kindness are unsurpassed and his cerebral horsepower formidable. #Wow #ZKSS! 😉 #Best2ALL!
Cross posting new white paper shared by #BIGGER 😉 ThankYOU!
Author: bigger Comment:
ProMIS just published a White Paper. Must read. https://promisneurosciences.com/2016site/wp-content/uploads/2018/01/v.final_.draft_.-White-Paper-LMW-toxic-oligomers.pdf
Comment Link: https://www.stockgumshoe.com/reviews/breakthrough-technology-alert/solving-ray-blancos-alzheimers-disease-is-now-completely-treatable-teaser/comment-page-1/#comment-4970031
Sharing and Caring in the #Gummunity! #Best2ALL!
#Alzheimers Article in The Atlantic by Olga Khazan
“The Startling LinkBetween Sugar and Alzheimer’s ”
https://www.theatlantic.com/health/archive/2018/01/the-startling-link-between-sugar-and-alzheimers/551528/
Best!
#ThankYOU Dara!
https://www.stockgumshoe.com/2018/01/the-twelve-biotechs-of-christmas-2018-balthasar/comment-page-7/#comment-4970759
#Sharing and Caring with the Gr8Gummunity!
#AD – PMN.to NP – As someone who lost their father to alzheimer’s disease, I did a fair bit of research into this company in the fall of 2016. I soon learned that I was in over my head, and humbly turned to Doc for help. In typical fashion, he gave generously in his response, and I learned much from it. And so I kept his words in my alzheimer’s file for future reference. Here is what he said on 8 August, 2016: Quote:
I have been peripherally aware of ProMIS for a few months. I do have an opinion on it, and I want to “bait” you into it gradually.
For as long as medicine has existed, it has confused manifestation of disease with disease itself. The fever accompanying a robust virus infection has often been regarded, especially in earlier times, as tantamount to the illness itself….and one so easily subdued that most people think quelling a fever is helping an infection. It may help a patient feel better—fevering is highly unpleasant—but latter data demonstrate that conquering the fever merely prolongs the infectious illness. For example, you can do surgery on many fowl without sterile technique because their body temperature is too high for Gram-positives to survive.
If the headache is a manifestation of a brain tumor, it does no good except achieving comfort to relieve the headache. It does literally no good to make a gastric ulcer heal using acid suppression if you do not kill the bacteria that caused the ulcer. The ulcer in fact is a defense front wielded to fight the bacteria in question. You might be able to drive away the hard chancre lesion that appears on the penis of a man with primary syphilis using steroid creams, but trust me, you have not helped the patient in the slightest by doing so. What’s at issue in these cases and 50 more like them is taking the jauntiest, most demonstrative manifestation of the disease, presuming that manifestation is the cardinal process….whereby the red herring you’ve been chases causes you to drive the patient right over a cliff with the best of intentions. I was once on hand in Indonesia to meet a fellowbacker who had fallen ill with a febrile illness. He’d gone to some pharmacist with a shingle who’d obtained a drop of blood and concluded his problem was “too many white cells.” Silly sod, of course. He had too many white cells because he had bacterial pneumonia, and when the pharmaquack gave him a retch-and-puke cancer chemotherapeutic to literally kill off his white cells, he had gotten very ill indeed, both from the medicine and from overwhelming sepsis. Proper antibiotics saved his life.
We are at a crossroads in Alzheimers between those who view plaque as the disease itself, and those who view it as manifestation of another, more primary cause. I am strongly in the latter camp (you might consider reading our article “The Manchurian Candida.”). All attempts at attacking plaque itself have afforded no therapeutic benefit at all, and I suspect that’s what the future perennially holds. With a sincere straight face, I would ask Cashman et al: so you’ve made sexy novel antibodies to plaque. What of it? Supposing your antibodies do in fact cross the blood brain barrier and get to the plaque. Will you be happy if they stick to it? Because see I won’t. How will that help the plaque? How will it do anything but intensify the pathology, making it one big 50-car protein pileup in the brain? You had thought of that hadn’t you Dr. Cashman? Antibodies go and stick to things, but since the thing you aim to have them stick to is fixed and embedded gunk, you can hardly expect your antibodies to create a cleansing flotsam in the brain and wash away the Alzheimer’s, can you?
And from there their proposal just goes limp.
I believe the plaque is there because of its robust anti-Candida activity, and that chronic subacute brain infection with Candida torulopsis is the origin of Alzheimers. It has much strong work to support it. Meanwhile, Cashman’s brains, the anti-Candida activity in their plaque now neutralized by sexpot antibodies, succumb even more quickly to the inflammation and toxic cytokine soup incurred by the Candida, and neurons die apace.
I wish ProMIS well, but it’s not a stock I would touch. If you want to donate money to Alzheimers research, seriously consider giving it to Carrasco in Spain, and if you want to invest in it, we are seriously watching the horizon waiting for a worthy company. We watch the horizon very closely, I can assure you….and the company just ain’t there yet.
Unquote Author: Ashton Comment: #ThankYOU Ashton for re-posting
Comment Link: https://www.stockgumshoe.com/2018/01/dr-kss-liveblog-noblecon-14/comment-page-1/#comment-4970866
#AD – Brain ‘pacemaker’ for Alzheimer’s http://www.bbc.com/news/health-42857576
#AD – #1 = I love you!
Ten Commandments for effective #Alzheimers/#dementia communication.
https://twitter.com/LEAD_Coalition/status/959772961967345665
#AD – Focus on what people living with #dementia can do (rather than what they cannot) https://twitter.com/LEAD_Coalition/status/960898125379481601
Family Caregiving for People With Dementia Infographic
http://www.prb.org/Multimedia/Infographics/2016/infographic-dementia.aspx#.VtSz4deuC58.twitter
#AD – Scientists toss another Alzheimer’s program into the scrap heap as PhII fails https://endpts.com/scientists-toss-another-alzheimers-program-into-the-scrap-heap-as-phii-fails/
#AD – BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions http://jem.rupress.org/content/early/2018/02/13/jem.20171831
ty https://twitter.com/OneMdcn/status/963811474065035266
#AD – The FDA raises hopes for Alzheimer’s drugs with a new set of draft rules. But are they going too far? https://endpts.com/the-fda-raises-hopes-for-alzheimers-drugs-with-a-new-set-of-draft-rules-but-are-they-going-too-far/? #Best2ALL!
#AD – Arthritis drugs could halve the risk of Alzheimer’s disease, study suggests http://www.telegraph.co.uk/news/2018/02/12/arthritis-drugs-could-halve-risk-alzheimers-disease-study-suggests/