Canadian neuroscientists say daily ibuprofen can prevent Alzheimer's disease
As a result, with as little as one teaspoon of saliva, it is possible to predict whether an individual is destined to develop Alzheimer's disease. This gives them an opportunity to begin taking early preventive measures such as consuming non-prescription non-steroidal drugs (NSAIDs) such as ibuprofen.
"What we've learned through our research is that people who are at risk of developing Alzheimer's exhibit the same elevated Abeta 42 levels as people who already have it; moreover, they exhibit those elevated levels throughout their lifetime so, theoretically, they could get tested anytime," says Dr. McGeer. "Knowing that the prevalence of clinical Alzheimer's Disease commences at age 65, we recommend that people get tested ten years before, at age 55, when the onset of Alzheimer's would typically begin. If they exhibit elevated Abeta 42 levels then, that is the time to begin taking daily ibuprofen to ward off the disease.
This article seems like an incredbile overstatement of the science behind the actual published article. (See below). I don't see how Dr. McGeer has shown that it is possible
whether an individual is destined to develop
The researchers who are spending 5 years of a clnical trial to test my blood, see my MRIs and PET scans, judge my cognition, and collect ALL my health records (yes, I did just have a shot of botox documented for a clinical trial!) can only "predict" that my "destiny" is a 30-60% chance of AD based on my Apoe 4/4 status.
For Dr. McGeer to claim that if I had only taken a daily ibuprofen starting 10 years ago I could "ward off" AD is irresponsible: I would ask him to show the clinical, observational, prospective or restrospective study that shows that correlation, much less showing that all other confounding variables that might "ward off" AD have been accounted for. https://www.eurekalert.org/pub_releases/2018-03/ip-cns032618.php
In fact, in writing, all he claims is to have found a possible PREDICTOR of RISK.
Here's a bit of the actual abstract (I didn't have access to the entire article.)
We then quantitated the Aβ42 in a series of samples with ELISA type tests. Control cases showed almost identical levels of salivary Aβ42 regardless of sex or age. All AD cases secreted levels of Aβ42 more than double those of controls. Individuals at elevated risk of developing AD secreted levels comparable to the AD cases. The results establish that salivary Aβ42 levels can be used to diagnose AD as well as to predict the risk of its future onset.
Questions: How many patients? How were they selected? Were scientists "blinded" as to who was healthy and who had MCI? what does "comparable" mean in any statistically significant sense? What was the "confidence interval?"
My translation of the last sentence: Levels of beta amyloid in people at risk of AD [that would include me, as a 4/4] can be used to predict that they are at risk of AD. Nothing in this review proves that these people go on to develop AD, and that this is in fact a proven, prospective biomarker. My biomarker for Lp(a) "proves" that I am at a statistical risk of aortic stenosis and coronary artery disease right now! My coronary calcium scan shows that my cardiac age is 39, and I have zero calcium. Biomarkers are not the same as outcome events! Sometimes they are not even valid biomarkers; they are just data points.
And there's nothing in the abstract, or any other research article I could find published in the last 8 years, that tied salivary function and AD to taking a daily ibuprofen to ward it off.
Here's a fall 2017 article that seems to be saying that many salivary functions ("homeostatis" and "impaired..function of the salivary glands" are associated with dementia.Antioxidant Defence, Oxidative Stress and Oxidative Damage in Saliva, Plasma and Erythrocytes of Dementia Patients. Can Salivary AGE [Advanced Glycation Endmarkers] be a Marker of Dementia? https://www.ncbi.nlm.nih.gov/pubmed/29053628
We show that in dementia patients the concentration/activity of major salivary antioxidants changes, and the level of oxidative damage to DNA, proteins and lipids is increased compared to healthy controls...In conclusion, dementia is associated with disturbed salivary redox homeostasis and impaired secretory function of the salivary glands. Salivary AGE may be useful in the diagnosis of dementia.
Finally, this is a summary of the state of the research on saliva biomarkers (among others mentioned in a larger article) in the fall 2017 EPMA Journal, which described itself as "a journal of predictive, preventive and personalized medicine (PPPM)" . Specific protein biomarker patterns for Alzheimer’s disease: improved diagnostics in progresshttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607150/
Recent comprehensive reviews on AD biomarkers exist , and specifically about saliva, suggesting early diagnosis of MCI and AD based on salivary lactoferrin, an iron- and also Aβ-binding glycoprotein.
It should be noted that the literature on saliva biomarkers for AD is still very limited (42 articles are currently available on PUBMED for saliva and Alzheimer’s), however, for the purpose of this review and future improved diagnostics it is worth mentioning some, as follows.
As a starting point, saliva is believed to be essential for the preservation of oral health and function, thus, unstimulated and stimulated submandibular salivary gland secretions were collected from non-medicated and otherwise healthy patients suffering from dementia and of the AD type (early disease stages) and compared to age-matched healthy controls. Results showed significantly lower salivary flow rates in the dementia sufferers, suggestive of a selective impairment in submandibular gland function in essentially healthy patients with early-stage dementia. ...
In general related to body fluids, future studies are warranted combining proteomics, metabolomics  and genomic evaluations with large cohorts.