Best shot for prevention is when you know what causes the disease.

I wasn't aware there is such a theory. What is it called?

This statement: was found in Alzheimer's facts and figures - http://www.alz.org/ video presentation at the end of the site:

http://youtu.be/In1IJocVor8

That is the point: how can we can say that Alzhemer's is not preventable, is we do not know all the aspects (even basic ones) of the disease yet?

I went to the Alz.Org website mentioned above and found the video. Yes, it indeed says Alzheimer's is "THE ONLY" disease without a means of prevention or cure. Also notice though that under "We advocate" (first page) it says

"As the largest, private non-profit funder of Alzheimer's research, the Association is committed to accelerating progress of new treatments, preventions and ultimately, a cure. Through our partnerships and funded projects, we have been part of every major research advancement over the past 30 years. Visit our online Research Center."

So they do believe in prevention. Fact is, Alz.Org wants very badly to raise money to increase awareness of the disease. Prevention is another matter. Like so many other diseases - pancreatic cancer? liver cancer? plain old dementia? - there may not be a way to prevent or cure it.

THINK FOR A MOMENT- IF ALZHEIMER'S DISEASE IS TRULY NEITHER PREVENTABLE NOR CURABLE, WHY RAISE MONEY AT ALL EXCEPT FOR PALLIATIVE REASONS? ACCORDING TO THEIR OWN VIDEO, ALZ.ORG NEEDS TO GET OUT OF THE BUSINESS OF RAISING MONEY FOR RESEARCH AND RAMP UP COMMITTMENT TO PROVIDING SERVICES TO VICTIMS OF THE DISEASE.

I don't think though that the idea is formulated as a theory. For the latest arguments on the whole idea of prevention, please see "preventive medicine" on wikipedia. That will give you a start. Good luck.

That contradiction is my point (there is no theory about this of course) and they can´t just say that is not preventable to raise money, they could say "it can be preventable if we start in middle age or in a MCI stage let´s raise money for that, but not close prevention strategy. Because now there is evidence in favour to prevention in many observational studies.

Agree, Andre - thanks for pointing this out. The video is misleading.

And thank you for your interest and courtesy.

I was not aware of this video, thanks for posting. I am an idealist that is slowly becoming a realist. I will admit that I am skeptical that there will be a "cure". AD is just too multifactorial to hope for a magic pill. As you indicated above, the best chance at prevention is identifying modifiable risk factors. We will need to target prior to onset or find what slows the disease.

Here is a new paper from a highly reputable source, that seems to agree with the "not preventable" thesis.

Science. 2012 Sep 21;337(6101):1488-92.

Preventing Alzheimer's disease.

Selkoe DJ.

Source

Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. [email protected]

Abstract

Despite intensive laboratory and clinical research over three decades, an effective treatment to delay the onset and progression of Alzheimer's disease is not at hand. Recent clinical trial failures suggest that we must treat the disease earlier than in its mild to moderate stages, and major progress in validating presymptomatic biomarkers now makes secondary prevention trials possible. We will learn more about the natural history of the disease and any partial therapeutic responses from detailed analyses of recent trial results. This process will likely position the field for success, but only with much greater investment in all aspects of Alzheimer research and with careful design of future trials.

Thanks a lot Carol, I will read this article, but he is talking about treatment and suggesting that only from now on we can talk about secondary prevention with the biomarkers. Well, if before the biomarkers we can not make clinical trials for prevention because we can not determine what is Alzheimer's or not...how he can say that there is no treatment? This text is contradictory. And we don´t know yet for sure if Alzheimer's phisiopathology is a cause or a consequence, so biomarkers can be "just" biomarkers.

Is there any data about the effect of preventive measures on AD in humans? Possibly not, but concerning sporadic AD and the putative effct of vascular risk factors a need for such studies has now emerged (see: Gorelic et al. Vascular contributors to cognitive decline and dementia. A statement for Healthcare Professionals From the American Heart Association/American Stroke association. Stroke 2011, 42:2672-2713). That statement says/suggests:... "“Long-term vascular risk marker* interventional studies beginning as early as midlife may be required to prevent or postpone the onset of VCI and Alzheimer disease"... It seems however that it takes quite a long time to get any results...

For familial AD (human) mutation in the genes for presenilin 1 and 2 and APP (with autosomal predominant inheritance), genetic counseling could be regarded as a form of prevention. It of course necessitates the previous identiciation of the mutation.

Here is an article that demonstrates reduced risk of AD in a f/u of 3.9 years: "Food combination and AD Risk" Arch Neurol 2010; 67:699-706. Gu and others showed that eating a Mediterranean diet could lower the risk for developing AD symptoms in a group of elderly subjects who were at risk for this disease.

Thank you, Linda! I was'nt awarwe of that study. Albeit there were some limitations that possibly cannot be avoided , such human studies are most valuable, as they may open up novel perspectives on AD.

We have to remember that Bowler and others showed us in 1998 that many "AD" patients have mixtures of both AD and vascular disease. Low ejection fractions in those with heart failure correlate well with reduced verbal memory (see Festa et al, Arch Neurol, 68:1021-1026, 2011). We also see extensive white matter disease and lacunar infarcts in some dementia patients (Jokinen et al, Neurology, 76:1872-1878, 2011). Instead of having a negative attitude, we need to take a very positive attitude with our AD patients, counseling them about diet, exercise, and giving them stroke prevention medications, if it is indicated.

I fully agree. It is interesting that many ofl those modifiable factors you mentioned somehow relate to vascular systems. And vascular systems seem/are suggested now to contribute AD pathophysiology (Nicoll JA, et al., Cerebral amyloid angiopathy plays a direct role in the pathogenesis of Alzheimer's disease. Pro-CAA position statement. Neurobiol Aging 2004;25:589,97, and Zlokovic BV. Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders. Nature Reviews Neuroscience. 2011; 12: 723-738), in addition to "vascular" dementia and in impaired memory function, as you mentioned.

Thank you Maarit and Linda for your responses, sorry for may delay to answer. I would like to add that populational studies can contribute to this issue:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0044239

This is an interesting article showing another angle of this complex disease.

Older Men Who Use Computers Have Lower Risk of Dementia is the title of the article

As Melissa pointed out, AD is multifactorial, and it is helpful to know that this kind of human studies have already been carried out. The study Andre mentioned was maybe not adjusted for vascular risk factors but of course is still thought-provoking. However, there is a need for similar kind of human studies to understand human AD, and possibly the "statement" by American heart association (encouraging to perform interventional studies on AD/dementia) can be seen in a wider perspective (any kind of "risk factors" to be studied).

Kivipelto and others in Sweden (Arch Neurol 62:1556-1560, 2005) did a large (n=1449), longitudinal (21 years) study of cardiovascular risk factors and showed that midlife obesity, high cholesterol and high systolic BP each increased the risk of AD by a factor of about 2. Each of these risk factors was additive, so that the odds ratio for all three risk factors was 6.2. Whitmer and other (Neurology 64:277-281, 2005) have found similar results in patients in this country.

One of the problems in all the literature is that some articles use the term "Alzhemier's" for all dementias including vascular and fronto-temporal. Vascular has a lot of preventive options pertinent to atherosclerotic vascular disease, of course.

Good observation, Vikki. Alzheimer's seems to be ill-defined and we need a clear, accurate definition of Alzheimer's Disease that differentiates it from all the other forms of dementias. Too often as you point out the term is used in a fashion that confuses issues of diagnosis, treatment and prevention.

Dear Alan and Vikki that´s the spirit of my question, This ill-defined condition is paralyzing the development of preventive measures against dementia.

In Improving Alzheimer’s disease phase II clinical trials

Barry D. Greenberg, et al (Alzheimer's & Dementia: The Journal of the Alzheimer's Association Volume 9, Issue 1 , Pages 39-49, January 2013) Concluded that "None of the disease modification trials completed thus far has been successful. The societal impact of continuing to fail in developing disease-modifying drugs for AD is enormous: If nothing is done to prevent or slow the disease, the worldwide prevalence of dementia is expected to increase to 65.7 million by 2030 and 115.4 million by 2050 [77], precipitating a major global economic crisis." Also considered that "Although clinical trials in preclinical cohorts are likely to be expensive and difficult to implement, this approach may be less costly or problematic than ongoing failed or uninformative trials of patients with mild-to-moderate AD"

But in other recent article at the same Journal Alzheimer's & Dementia: The Journal of the Alzheimer's Association Volume 9, Issue 1 , Pages 63-75.e2, January 2013

The global prevalence of dementia: A systematic review and metaanalysis .Martin Prince et al shows a graphic about the growth in numbers of people with dementia in high-income (HIC) and low- and middle-income countries (LMIC) This figure displays a different increasing rhythm, lower in high income countries (usually with higher life expentancy) so we might infer that better diet, health plannings, and quality of life parameters affects dementia (in general - not specificly Alzheimer) incidence.

Thank you Javier (Xavier in portuguese!!) We found a very similar information in ELSA - English Longitudinal Study on Ageing, our article is about to be published.

Will be a very interesting reading, André. Please tell us when and where is going to be publish!

Look at the paper by Deschaintre and others (Neurology 2009;73:674-680), where a group of 301 consecutive AD patients without CVD was followed over 6 years. Baseline MMSE scores were similar in all three groups. Those who had vascular risk factors (VRF) managed carefully had a slower cognitive decline than those who had some VRF treated or no VRF treated (BP, HLD, DM, smoking, etc).

A dissident's view:

The scientific community has more or less unanimously set the goal in developing a "disease modifying" medication for alzheimer's. Running to find shortcuts is not actually equal to following the scientific paradigm.

No wonder Alzheimer's disease is ill-defined.

I am sending to your attention updated information on the matter.

Telomere Length Shortening and Alzheimer Disease—A Mendelian Randomization StudyYiqiang Zhan, MD1; Ci Song, PhD1; Robert Karlsson, PhD1; Annika Tillander, PhD1; Chandra A. Reynolds, PhD2; Nancy L. Pedersen, PhD1; Sara Hägg, PhD1

[+-] Author Affiliations 1Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden

2Department of Psychology, University of California, Riverside

JAMA Neurol. 2015;72(10):1202-1203. doi:10.1001/jamaneurol.2015.1513.

Role of Infection in Alzheimer's Ignored, Experts Say

Nancy A. Melville

| March 18, 2016

The potentially critical role of infection in the etiology of Alzheimer's disease is largely neglected, despite decades of robust evidence from hundreds of human studies, as well as the possible therapeutic implications, experts say.

"Despite all the supportive evidence, the topic [of linking infections to Alzheimer's disease] is often dismissed as 'controversial,' " the authors of an editorial, signed by an international group of 33 researchers and clinicians, write.

                                                                                      Chicken or the Egg?

Commenting on the editorial for Medscape Medical News, Richard B. Lipton, MD, Edwin S. Lowe Professor, vice chair of neurology, and director of the Division of Cognitive Aging and Dementia at Albert Einstein College of Medicine in New York City, applauded the effort to raise awareness of the issue.

"The authors are to be commended for reminding us of the hypothesis that infection may contribute to Alzheimer's disease," he told Medscape Medical News.

He noted the variety of genetic and environmental factors that can influence onset and progression of complex disorders such as Alzheimer's disease.

"For Alzheimer's disease, most people would agree that cardiovascular risk factors, traumatic brain injury, and stress increase risk of disease," he said.

"It is entirely plausible that infectious agents may be one of many factors that contribute to the development of Alzheimer's disease. Infectious agents could operate through several mechanisms."

The evidence does not necessarily prove a causative role, he added.

"Temporality means that infection precedes disease," he said. "The studies showing infectious and inflammatory markers in the Alzheimer's brain don't tell us which came first. Alzheimer's disease could be a state which predisposes to infection."

The editorialists' financial disclosures are available online. Dr Lipton has disclosed no relevant financial relationships.

J Alzheimers Dis. Published online March 8, 2016. Editorial

Read the work from the Nun Study......and the Rush Presbyterian Aging Study.  Both studies showed that we can have Akzheimer changes in our brains at autopsy and yet be "healthy" (not demented) at the time of death if we are careful to control for vascular risk factors (HTN, smoking, DM) and prevent ourselves from developing stroke (even a small stroke can precipitate cognitive decline in someone with AD in the brain). 

See Schneider et al Ann Neurol 2007;62:59-66

Scientists find tau protein as better marker of Alzheimer's disease 

A buildup of plaque and dysfunctional proteins in the brain are hallmarks of Alzheimer's disease. While much Alzheimer's research has focused on accumulation of the protein amyloid beta, researchers have begun to pay closer attention to another protein, tau, long associated with this disease but not studied as thoroughly, in part, because scientists only recently have developed effective ways to image tau.

Genetic risk score may help detect Alzheimer's disease risk in healthy young adults 

New research shows that a genetic risk score may detect those at higher risk for Alzheimer's disease long before symptoms appear—even possibly in healthy young adults, according to a study published in the July 6, 2016, online issue of Neurology, the medical journal of the American Academy of Neurology.

Scientists discover gene that may open new door to developing treatments for Alzheimer's diseaseScientists discover gene that may open new door to developing treatments for Alzheimer's disease

Scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have identified a gene that may provide a new starting point for developing treatments for Alzheimer's disease (AD).