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This is a response in a previous thread, but it was part of a...

  1. 29 Posts.
    This is a response in a previous thread, but it was part of a conversation that was leading into a different topic, and so I thought I'd highlight it under its own topic:

    ~~~~~~~

    I appreciated several of Tanzi's recent talks in which he made distinctions between the definition of Alzheimer's (a medical definition having to do with a certain set of characteristics) and dementia per se.

    Here's a good definition of dementia (which is distinct from various possible causes of it):

    "Dementia is the loss of mental functions such as thinking, memory, and reasoning that is severe enough to interfere with a person's daily functioning. Dementia is not a disease itself, but rather a group of symptoms that are caused by various diseases or conditions."

    As Tanzi stated it, ***by definition*** Alzheimer's includes plaques and tangles in association with dementia. But AD is not one and the same with "dementia."

    He went on to talk about it in this way:

    A person can have plaques and/or plaques and tangles, and never get to dementia, and there are various reasons for that, some of which he described. People can get to dementia without having plaques, some reasons for which, he also talked about.

    One of the things he talked about was inflammation, which entails oxidative stress, just as you (Lane) mentioned, which, in and of itself, can do terrible damage, and doesn't necessarily follow from earlier plaque build-up.

    ~~~~~~

    However (and this is where AD in particular comes in), he also stressed that one significant way in which dementia can come about, and seems to be a common way in which it does, is by the long-term build-up of amyloid as plaques, which can then lead to tangles (and cell death and inflammation, the last step of which is a very significant killer of cells, and revs up the other stages even more - when a kind terrible positive feedback loop comes into play).

    As he says it, that slow build-up of plaque (via amyloid aggregation) is ONE way in which the "fire" of cell death (via tangles) is lit, BUT NOT THE ONLY WAY. And that PARTICULAR PATHWAY to dementia would be diagnosed as Alzheimer's Disease.

    And for those studying Alzheimer's Disease in particular, which by definition, does include a build up of plaques and tangles... they are trying to understand how those conditions relate...

    The biggest question (for years and years) being... does plaque/amyloid build-up LEAD TO tangles? (That's not a question of whether other things also lead to tangles - which is already clear, they do - or whether or not plaques and tangles are often seen together - they are - but specifically a question about whether or not amyloid *leads to*/*causes* tangles.)

    ~~~~~~

    Of course, that's why the recent work from Tanzi's lab, the "AD in a dish," is so significant for those considering that question. It apparently has provided an important proof of concept showing a direct, step by step, relationship between plaques and tangles (and from early conditions of excessive a-beta - which could be caused by either excessive production or problems with clearing).

    That's the extent of the model so far, but it's already helped to answer one of the most important questions in AD studies regarding how a-beta and tangles are related. "Does plaque lead to/cause tangles?" This model shows that, "Yes, it does."

    And Tanzi is sharing the model so that the work can be replicated and further tested. He's also working hard to build it out so that more conditions can be tested. For instance, he wants to add glial cells and a blood/brain barrier, etc.

    ~~~~~~

    So I would agree with you that there are other significant ways in which pathology in the brain can lead to dementia, ways in which plaques aren't needed for dementia to occur. And a lot of folks - including those working on understanding AD in particular - are apparently very interested in oxidative stress and inflammation, a key interest of yours.

    But I do think it's looking more and more likely that amyloid buildup over time IS one significant way in which pathology leading to dementia can happen, one way in which the "fire" of neurodegeneration can be lit. And that particular way, in which amyloid plaques & tangles are present and play key roles, would, by definition, be Alzheimer's.

    ~~~~~~

    I think Tanzi's analogy of cholesterol build up and heart disease makes a lot of sense. Of course, the key is to prove that to be the case. And a lot of people think that Tanzi's lab has begun to do just that.

    Linda
    Last edited by latebloomer: 14/11/14
 
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