Stories
Slash Boxes
Comments

SoylentNews is people

posted by martyb on Friday November 03 2017, @02:22PM   Printer-friendly
from the progress-against-a-nasty-disease dept.

https://news.ubc.ca/2017/10/31/alzheimers-disease-might-be-a-whole-body-problem/

Alzheimer's disease, the leading cause of dementia, has long been assumed to originate in the brain but new research indicates that it could be triggered by breakdowns elsewhere in the body.

The findings, published today in Molecular Psychiatry [DOI: 10.1038/mp.2017.204] [DX], offer hope that future drug therapies might be able to stop or slow the disease without acting directly on the brain, which is a complex, sensitive and often hard-to-reach target. Instead, such drugs could target the kidney or liver, ridding the blood of a toxic protein [amyloid-β protein] before it ever reaches the brain.

"Alzheimer's disease is clearly a disease of the brain, but our research shows that we need to pay attention to the whole body to understand where it comes from, and how to stop it," said Dr. Weihong Song, UBC psychiatry professor.


Original Submission

 
This discussion has been archived. No new comments can be posted.
Display Options Threshold/Breakthrough Mark All as Read Mark All as Unread
The Fine Print: The following comments are owned by whoever posted them. We are not responsible for them in any way.
  • (Score: 1, Informative) by Anonymous Coward on Friday November 03 2017, @04:21PM (4 children)

    by Anonymous Coward on Friday November 03 2017, @04:21PM (#591715)

    Along with a chorus of others, we have previously argued against the assumption that Aβ accumulation is the primary early pathogenic trigger of AD [4]-[8]. An unintended consequence of that assumption, which contributes to the continued failure of anti-amyloid clinical trials, is that affirmative diagnosis of AD-type dementia can only occur when the presence of Aβ accumulation in the brain is confirmed. However, recent imaging studies confirm previous observations of Aβ accumulation in a significant proportion of non-demented individuals [4],[9],[10]. Conversely, a sizable proportion of patients clinically diagnosed with AD do not display Aβ accumulation-even though neurodegeneration is in progress [4],[11]. Remarkably, rather than concluding that Aβ status is not a reliable marker for the early stages of clinical AD, a consensus has been reached in which clinically diagnosed AD patients without Aβ are classified as not suffering from AD.

    https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-014-0169-0 [biomedcentral.com]

    Starting Score:    0  points
    Moderation   +1  
       Informative=1, Total=1
    Extra 'Informative' Modifier   0  

    Total Score:   1  
  • (Score: 2) by frojack on Friday November 03 2017, @08:25PM (3 children)

    by frojack (1554) on Friday November 03 2017, @08:25PM (#591853) Journal

    Remarkably, rather than concluding that Aβ status is not a reliable marker for the early stages of clinical AD, a consensus has been reached in which clinically diagnosed AD patients without Aβ are classified as not suffering from AD.

    That wouldn't be the first time that has happened in the field of medicine.
    There are more than a few very common diseases where diagnosis is just wrong. [cnn.com]
    Yet these guys write that is if recognizing the misdiagnosis is somehow a bad thing.

    Behavioral based diagnosis is a tricky business at best. Deciding that Neurodegeneration is in progress really says nothing about the source. If AD is defined as the presence of Aβ accumulation, AND Aβ accumulation is missing, then what would be the point of continuing to treat Aβ accumulation?

    --
    No, you are mistaken. I've always had this sig.
    • (Score: 0) by Anonymous Coward on Friday November 03 2017, @10:12PM

      by Anonymous Coward on Friday November 03 2017, @10:12PM (#591905)

      There doesn't seem to be any point of continuing to treat Aβ accumulation... that is the point.

    • (Score: 2) by TheLink on Saturday November 04 2017, @08:55AM

      by TheLink (332) on Saturday November 04 2017, @08:55AM (#592113) Journal

      I doubt it'll work for everybody (lots of other causes for dementia) but it may work for lot of people. After all many people have type 2 diabetes, so while not all dementia might be "type 3 diabetes" a large percentage might be:
      https://www.nia.nih.gov/alzheimers/clinical-trials/study-nasal-insulin-fight-forgetfulness-sniff [nih.gov]
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3260944/ [nih.gov]
      http://www.alzforum.org/therapeutics/nasal-insulin [alzforum.org]

      I don't recommend you DIY and bypass professional medical treatment, but hey if you're getting desperate the side effects may not be bad enough for you:
      http://www.lostfalco.com/intranasal-insulin/ [lostfalco.com]

    • (Score: 1) by rylyeh on Saturday November 04 2017, @05:39PM

      by rylyeh (6726) <{kadath} {at} {gmail.com}> on Saturday November 04 2017, @05:39PM (#592222)

      Amyloid-β is definatley not even the biggest problem: Gene variant linked to Alzheimer’s disease is a triple threat [sciencenews.org]

      For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood.

      But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles.
      Death sentence

      Mouse brain nerve cells (green) making a disease-causing version of the tau protein were grown in lab dishes with supporting brain cells called glia. The glial cells produced different versions of the human APOE protein, or had no APOE. Glia making the APOE4 version of the protein often killed the nerve cells (bottom right).

      Y. Shi et al/Nature 2017

      In one experiment, mice that had no A-beta in their brains developed more tau tangles if they carried the human version of APOE4 than if they had the human APOE3 gene, Holtzman and colleagues found. That finding indicates APOE4 affects tau independently of A-beta.

      Brains of people who died from various diseases caused by tangled tau had more dead and damaged cells if the people carried APOE4. The researchers also tracked 592 people who had low levels of A-beta in their cerebral spinal fluid — a clue that plaques have formed in the brain — and who showed symptoms of Alzheimer’s. Over a five- to 10-year period, the disease progressed 14 percent faster in people with one copy of APOE4 and 23 percent faster in people with two copies than in people who didn’t have that version of the gene, the researchers found. Those worsening symptoms are presumed to be caused by more rapid buildup of tau tangles in the APOE4 carriers.

      APOE4 also seems to make Alzheimer’s worse by causing inflammation, the researchers found. Two kinds of mouse glial brain cells, microglia and astrocytes, making different versions of the APOE protein were grown with brain nerve cells, or neurons, that make disease-causing forms of tau. Mouse neurons grown with glia making no APOE grew well, even though they were making abnormal tau. But neurons grown with glia making APOE4 often died. APOE4 provoked inflammation responses in the normally friendly astrocytes and microglia, leading those cells to kill neurons, the researchers found. Such inflammation can make brain degeneration worse.

      Based on the above research - I think these 'new treatments' will prove to be ineffective.

      --
      "a vast crenulate shell wherein rode the grey and awful form of primal Nodens, Lord of the Great Abyss."