Supposed Alzheimers Plaques Show Up In Clear Thinking Aged People

[ecstatichamster]

Don't have a study as this was just presented:

https://www.sciencedaily.com/releases/2016/11/161116132813.htm

But surprising new Northwestern Medicine research on the brains of individuals 90 years and older who had superior memories until their deaths revealed widespread and dense Alzheimer's plaques and tangles in some cases, considered full-blown Alzheimer's pathology.

"This is amazing," said Northwestern Medicine lead investigator Changiz Geula. "We never expected it. It tells us there are some factors that are protecting their brains and memories against the Alzheimer's pathology of plaques and tangles. Now we have to find out what those are."

The Northwestern findings are the first to indicate that full-blown Alzheimer pathology also can exist in brains of elderly who show superior cognitive performance.

Not surprisingly, the entire Alzheimer's treatment community will still be doing the same things, even though these amyloid-beta plaques probably have nothing to do with the problem.

 

[ecstatichamster]

this is VERY VERY important...it says that current theory about Alzheimers is completely wrong.

Old people who SHOULD have had terrible symptoms were sharp as a tack, even though their brains were full of this plaque that supposedly causes Alzheimer's.

 

[Dante]

There are 4-5 hypotheses floating around. Plauqes are involved in pathogeneis what exactly causes them is specualtive. Don't jump to conclusions that fast. As the study says, may be some environmental factor, diet might be protecting their hippocampus.

 

[haidut]

this is VERY VERY important...it says that current theory about Alzheimers is completely wrong.

Old people who SHOULD have had terrible symptoms were sharp as a tack, even though their brains were full of this plaque that supposedly causes Alzheimer's.

There is solid evidence that the beta-amyloid accumulation is adaptive and probably not nearly as pathogenic as the mainstream theory goes. This study shows that beta-amyloid can treat an animal model of MS and likely has other beneficial effects.
Accused of complicity in Alzheimer’s, amyloid proteins may be getting a bad rap, study finds

As usual, the presence of the beta amyloid may simply be a bystander effect while medicine considers it a villain. The cholesterol in arterial plaques and DHT in follicles of balding men are two other examples. Unfortunately, beta amyloid is a very convenient target for drug development and it is unlikely to go away any time soon as the official suspect in Alzheimers.

 

[ecstatichamster]

you wouldn't have the study URLs handy would you @haidut

This is fascinating. The whole theory is nonsense.

 

[haidut]

you wouldn't have the study URLs handy would you @haidut

This is fascinating. The whole theory is nonsense.

There are at least 3 studies by that group.
Amyloid Fibrils Composed of Hexameric Peptides Attenuate Neuroinflammation | Science Translational Medicine
Mechanisms of action of therapeutic amyloidogenic hexapeptides in amelioration of inflammatory brain disease. - PubMed - NCBI
Amyloid fibrils activate B-1a lymphocytes to ameliorate inflammatory brain disease

To me, the giveaway was this line from the Stanford page:
"...Taken together, the studies begin to suggest the radical new idea that full-length, amyloid-forming proteins may in fact be produced by the body as a protective, rather than destructive, force. In particular, Steinman’s study shows that these proteins may function as molecular chaperones, escorting and removing from sites of injury specific molecules involved in inflammation and inappropriate immune responses."

Peat does not miss a single chance to remind his listeners in every interview that the role of the immune system is NOT to attack pathogens and destroy tissue (as in autoimmune conditions). It is to clear up debris and maintain order - i.e. a force of morphostasis.
home_page

This is exactly what the Stanford people found the beta-amyloid to be doing and ironically it is also the reason why Alzheimer is being considered by some experts to be an "autoimmune" condition.

 

[ecstatichamster]

thanks, very helpful. Wow!

 

[Koveras]

you wouldn't have the study URLs handy would you @haidut

This is fascinating. The whole theory is nonsense.

There are at least 3 studies by that group.
Amyloid Fibrils Composed of Hexameric Peptides Attenuate Neuroinflammation | Science Translational Medicine
Mechanisms of action of therapeutic amyloidogenic hexapeptides in amelioration of inflammatory brain disease. - PubMed - NCBI
Amyloid fibrils activate B-1a lymphocytes to ameliorate inflammatory brain disease

To me, the giveaway was this line from the Stanford page:
"...Taken together, the studies begin to suggest the radical new idea that full-length, amyloid-forming proteins may in fact be produced by the body as a protective, rather than destructive, force. In particular, Steinman’s study shows that these proteins may function as molecular chaperones, escorting and removing from sites of injury specific molecules involved in inflammation and inappropriate immune responses."

Peat does not miss a single chance to remind his listeners in every interview that the role of the immune system is NOT to attack pathogens and destroy tissue (as in autoimmune conditions). It is to clear up debris and maintain order - i.e. a force of morphostasis.
home_page

This is exactly what the Stanford people found the beta-amyloid to be doing and ironically it is also the reason why Alzheimer is being considered by some experts to be an "autoimmune" condition.

There was also this one

Paradigm shift redefining molecular, metabolic and structural events in Alzheimer's disease involves a proposed contribution by transition metals. ... - PubMed - NCBI

"It is estimated that 5.5 Million North Americans suffer from varying degrees of Alzheimer's disease (AD) and by the year 2050 it may be one in 85 people globally (100 Million). It will be shown that heavy metal toxicity plays a significant role in sporadic AD. Although current literature speaks to involvement of metal ions (via Fenton reaction), studies and reviewers have yet to link cellular events including known structural changes such as amyloid plaque development to this metal toxicity the way it is proposed here. Contrary to the current AD model which positions BACE1 (β-secretase) as an aberrant or AD-advancing enzyme, it is proposed herein that the neuron's protective counteraction to this metal toxicity is, in fact, a justified increase in BACE1 activity and amyloid precursor protein (APP) processing to yield more secreted APP (sAPP) and β-amyloid peptide in response to metal toxicity. This new perspective which justifies a functional role for APP, BACE1 enzyme activity and the peptide products from this activity may at first appear to be counterintuitive. Compelling evidence, however, is presented and a mechanism is shown herein that validate BACE1 recruitment and the resulting β-amyloid protein as strategic countermeasures serving the cell effectively against neuro-impeding disease. It is proposed that β-amyloid peptide chelates and sequesters free heavy metals in the extracellular medium to aggregate as amyloid plaque while unchelated β-amyloid migrates across the cell membrane to chelate intracellular free divalent metals. The sequestered intracellular metal is subsequently chaperoned as a metallo-peptide to cross the plasma membrane and aggregate as amyloid plaques extracellularly. The BACE1 countermeasure is not genetic or metabolic aberration; and this novel conclusion demonstrates that it must not be inhibited as currently targeted. APP, BACE1, β-amyloid peptide, and sAPP play positive roles against the preclinical oxidative load that predates AD symptoms for as long as 20 years. A healthy neuron may tolerate free metal toxicity, such as iron in the case of injury-induced amyloid, for as long as twenty years due to this very BACE1 activity. In later stages, the uncontrolled metals and ROS are compounded by other factors which together overcome this BACE1/β-amyloid protein countermeasure. This results in a sudden increase in IL-1 leading to Tau's hyperphosphorylation as cited and eventually to Tau dissociation from the microtubule cytoskeleton interrupting cell trafficking. At this later stage of AD the β-amyloid protein which once served as a vehicle to escort toxic metals to the extracellular medium and a trap to form a relatively benign extraneuronal disposal site is no longer translocated due to interruption of trafficking and now accumulates intracellularly facilitating hyper-oxidative ROS levels and contributes to irreversible neuron apoptosis."