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"Age-related neurodegenerative diseases, like Alzheimer's, progress over a long period of time before they become clinically apparent. The earliest physiological and molecular events are largely unknown," said Mastroeni. "Findings from our laboratory have uncovered early expression changes in nuclear-encoded, but not mitochondrial-encoded mRNAs occurring in one's early 30s, giving us a glimpse into what we suspect are some of the earliest cellular changes in the progression of Alzheimer's disease."
Results of the new study show that specific classes of genes associated with mitochondrial cell respiration display reduced expression levels in patients with Alzheimer's disease, compared with normal patients.
The study also examines gene expression in subjects whose brains show an intermediate level of illness known as mild cognitive impairment. Here, the opposite effect is observed, with relevant genes exhibiting increased levels of expression. The authors suggest this observation may point to some kind of compensatory mechanism in the brain attempting to stave off the disease in its earlier stages.
Further, the study proposes that restoring a specific set of damaged genes linked to mitochondrial function and located in the nuclear DNA of cells may offer a promising strategy for halting the disease's advance.
Journal: Nuclear but not mitochondrial-encoded OXPHOS genes are altered in aging, mild cognitive impairment, and Alzheimer's disease. Alzheimer's and Dementia, 2016; DOI: 10.1016/j.jalz.2016.09.003
Simply put, the mitochondria run out of gas, and Alzheimer's follows.
(Score: 1, Informative) by Anonymous Coward on Friday November 11 2016, @06:18PM
I assure you this hypothesis was not pre-registered. They expected an intermediate level of expression in the people with mild impairment. What is happening here is that the results didn't fit their original "theory", but that "theory" was vague enough that they can indeterminately avoid refutation via liberal use of ad hoc explanations. And they are actually doing better than most medical researchers because at least we are told about the conflicting results.
When will people stop taking this stuff seriously? It is a joke.
(Score: 2) by RamiK on Friday November 11 2016, @07:54PM
Changing thesis statements to match observed results isn't done to boost the authors' ego. It's done to simplify paper's format and improve parsing and comprehension. You don't need to know what the experimenters initially assumed. You need to know the results they found, the model they propose to explain the results and the procedure to replicate their results.
Keep your cool eureka \ embarrassing duh moments to the tenure acceptance speech.
compiling...
(Score: 1, Touché) by Anonymous Coward on Friday November 11 2016, @08:04PM
Lets say you have a theory "Power outage in the brain is a source of Alzheimer's", then you collect data and see that there is actually more "power in the brain" in the Alzheimer's group.
So you keep the same theory but add an ad hoc qualifier: "Power outage in the brain is a source of Alzheimer's and this is masked by a compensatory mechanism". Do you think much progress will be made in understanding Alzheimer's using this method? I do not.
(Score: 1) by Zipf on Friday November 11 2016, @08:32PM
It means I am going to keep taking my riboflavin.
(Score: 2) by RamiK on Friday November 11 2016, @09:53PM
That's an oxymoron. Given the freedom to change the thesis to match the results, you'd still get a paper off saying "Alzheimer doesn't directly affect power in the brain" instead.
That's to say, you'd need a compensatory mechanism* to explain why the author needed a compensatory mechanism instead of changing the thesis... That's one dull razor.
*A third factor the likes of not wanting to deviate from the research grant proposal wouldn't be completely out of the question if this was some pharma research. But this is basic research so what's the point?
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(Score: 3, Informative) by sjames on Saturday November 12 2016, @10:21AM
I'm not sure what you're on about. They formed a hypothesis and tested it. The data said "not so fast", so they now have a new hypothesis that is consistent with the new data. As long as they then refine and test their new hypothesis, it's science at it's best.
(Score: 0) by Anonymous Coward on Friday November 11 2016, @08:05PM
Intranasal insulin might help get the gas get used:
https://www.ncbi.nlm.nih.gov/pubmed/17942819 [nih.gov]
https://www.ncbi.nlm.nih.gov/pubmed/25374101 [nih.gov]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4743662/ [nih.gov]
http://jamanetwork.com/journals/jamaneurology/fullarticle/1107947 [jamanetwork.com]
https://www.ncbi.nlm.nih.gov/pubmed/26401706 [nih.gov]
More here if you want a convenient overview:
http://www.lostfalco.com/intranasal-insulin-studies-on-cognitive-enhancement-alzheimers-traumatic-brain-injury-etc/ [lostfalco.com]
(Score: 2) by KilroySmith on Friday November 11 2016, @08:40PM
I just hope they figure out how to cure Alzheimer's by the time I
...
What was I saying?
(Score: 2) by TGV on Saturday November 12 2016, @07:42AM
It's one of the few hypotheses that sounds acceptable on first hearing. It would still have to explain why memories would fade, given that they are most likely hard-coded in the synaptic path ways, why plaque forms, and that it's not the other way around (i.e. plaque triggers reduction in expression), and why head injury seems to boost Alzheimer's, but it sounds worthy of further investigation.
(Score: 0) by Anonymous Coward on Saturday November 12 2016, @03:47PM
so, it's caused by incorrect diet as some nutritionists have suggested. get off the pig slop and start eating a high fat diet with veggies instead (with exercise) and all these high tech "genetic" illnesses will disappear. so will all the doctor's drug dealing profits so don't expect a lot of press and education for the young.