It is not. Vascular disease can also cause dementia, but it is a different kind.

Observational studies suggest some connection between vascular risk factors and Alzheimers, but RCTs do not confirm that treating vascular risk factors reduce the risk of Alzheimers. There might still be a modest vacular connection, or the whole phenomenon may be a genetic connection through APOE. Contrast that with other CVD and multi-infarct dementia, which is profoundly affected by treating vascular risk factors. Everybody gets Alzheimers changes if he or she lives long enough, but lots of people maintain normal BP, normal carotid intima thickness, and clean coronaries throughout the lifespan.

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.

The latest tests for early detection

Two studies explore potential new blood tests for Alzheimer's disease

Published on November 10, 2015 at 1:25 AM · No Comments

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There is increasing evidence that the brain changes of Alzheimer's disease begin decades before memory and thinking problems occur, prompting the need for better methods of early detection for this progressive, fatal brain disease. Consequently, there is a growing school of thought that the most effective future Alzheimer's drug therapies will be administered to those who are at high risk of the disease before cognitive symptoms appear.

To bolster development of a simple, inexpensive, noninvasive test that can detect the risk of Alzheimer's disease, the Alzheimer's Association, the Crnic Institute for Down Syndrome, and the Global Down Syndrome Foundation ("Global") are funding two studies of potential new blood tests for Alzheimer's, including one that uses just one drop of blood:

One study will evaluate whether examining changes in ribonucleic acid (RNA) found in one drop of blood can accurately identify people who will develop Alzheimer's in individuals with Down syndrome who are at high risk for the disease. The study is being led by Marwan Sabbagh, M.D., Director of the Alzheimer's and Memory Disorders Division at the Barrow Neurological Institute in Phoenix, and Matt Huentelman, Ph.D., Associate Professor in the Neurogenomics Division Unit at the Translational Genomics Research Institute in Phoenix.

Another study will test whether a specific set of blood proteins can identify who is at risk for developing Alzheimer's in a unique, high -risk population, individuals with Down syndrome. The study is being led by Nicole Schupf, Ph.D., M.P.H., Dr.Ph.H., Professor of Epidemiology at Columbia University Medical Center in New York City, and Sid O'Bryant, Ph.D., Director of the Center for Alzheimer's and Neurodegenerative Disease Research at the University of North Texas Health Science Center in Fort Worth.

"Prevention of Alzheimer's dementia may be more effective and easily achieved than attempting to treat the disease once symptoms already exist and irreversible damage to the brain has already occurred," says Dean Hartley, Ph.D., Director of Science Initiatives for the Alzheimer's Association. "For this approach to be successful, we must be able to simply and accurately assess risk early in the disease process. The Alzheimer's Association and the Global Down Syndrome Foundation hope that these two exciting projects drive that effort forward."

"Autopsy is still the only way to definitively diagnose Alzheimer's disease," said Michelle Sie Whitten, President and CEO of the Global Down Syndrome Foundation. "If these researchers are successful we will be one step closer to catching Alzheimer's in its early stages and hopefully then be able to treat people with the disease earlier and actually prevent dementia from occurring, when new treatment options become available."

The grant awards are part of $1 million in new funding for Down syndrome-related Alzheimer's disease research. Four projects will receive $250,000 each through the joint funding effort.

Nearly all adults with Down syndrome begin developing the brain changes of Alzheimer's in their 30s. By age 55 or 60, it is estimated 55-70% will develop dementia. Because people with Down syndrome are at high risk for Alzheimer's, answers to important research questions about the disease may be developed more quickly in this population than by studying people with sporadic, late-onset Alzheimer's, where symptoms appear most often after age 65 - and in many cases not until the 70s or 80s.

"It used to be common for individuals with Down syndrome to die in their 30s, but because of medical advances they are now regularly living into their 50s and 60s. The irony is that they are now facing dementia due to Alzheimer's disease," says Huntington Potter, Ph.D., Director of Alzheimer's Research at the Crnic Institute for Down Syndrome and a Professor of Neurology at the University of Colorado, Denver. "At the same time, questions about Alzheimer's may be answered more quickly by studying this disease in people with Down syndrome because of their high risk for Alzheimer's and the earlier onset. Through this approach, people with Down syndrome have the opportunity to further our understanding of Alzheimer's disease and we have the opportunity to help this population."

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Scientists are not sure exactly why individuals with Down syndrome are at high risk for Alzheimer's disease but past research shows that a gene on chromosome 21 codes for the amyloid precursor protein (APP) that gets cut into fragments that accumulate into the hallmark amyloid brain plaques of Alzheimer's. People with Down syndrome are born with an extra copy of chromosome 21.

"The hope for our study is that the identification of RNA biomarkers for Alzheimer's could be used in a non-invasive blood test that requires just one drop of blood to assess an individual's risk of developing the disease, similar to the way a person with diabetes checks their blood sugar," says Sabbagh. "If we can learn early on that a person is at risk, the goal would be to start preventative therapies immediately. This could be a game changer."

"Our research could provide new information about potential biomarkers, including protein changes detected in blood, that could more accurately and easily predict the risk for Alzheimer's disease in people with Down syndrome," says Schupf. "If successful, we believe there is a chance that these biomarkers could also be used to assess Alzheimer's risk in all groups of people."

The Alzheimer's Association is the largest nonprofit funder of Alzheimer's research, having awarded more than $350 million to over 2,300 projects since 1982. The Association currently supports more than 350 ongoing research projects in 21 countries totaling more than $82 million.

The Global Down Syndrome Foundation raises funds for the Crnic Institute for Down Syndrome to underwrite critical research benefiting people with Down syndrome. To date, $5.7 million in research grants has been given to 33 investigators.

The two other research projects the Alzheimer's Association and Global are funding through the joint grant award effort are:

A test of a potential Alzheimer's drug treatment that reduces levels of toxic protein fragments in the brain of a mouse model of Down syndrome. The project is led by William Mobley, M.D., Ph.D., Chair of the Department of Neurosciences at the University of California, San Diego (UCSD) and Executive Director of UCSD's Down Syndrome Center for Research and Treatment.

A study to determine whether a protein called Dyrk1A influences the build-up of brain proteins that lead to the formation of plaques and tangles that are key features of Alzheimer's in a mouse model of Down syndrome. Dyrk1A is created by one of the genes on chromosome 21 and is overabundant in the brains of people with Down syndrome. The study is led by Fei Liu, Ph.D., Head of Molecular Neuroscience for the Research Foundation for Mental Hygiene, Inc. at the New York State Institute for Basic Research in Staten Island.

Source:

Alzheimer's Association

Dear Marianne Levon Shah Varian

thank you very much for your interesting references

best regards

Dear Baptiste Lacoste

I sincerely appreciate your comments.

and references provided us

best regards

A Culture–Brain Link: Negative Age Stereotypes Predict Alzheimer’s Disease Biomarkers.

Levy, Becca R.; Ferrucci, Luigi; Zonderman, Alan B.; Slade, Martin D.; Troncoso, Juan; Resnick, Susan M.

Psychology and Aging, Dec 7 , 2015, No Pagination Specified. http://dx.doi.org/10.1037/pag0000062

Abstract

Although negative age stereotypes have been found to predict adverse outcomes among older individuals, it was unknown whether the influence of stereotypes extends to brain changes associated with Alzheimer’s disease. To consider this possibility, we drew on dementia-free participants, in the Baltimore Longitudinal Study of Aging, whose age stereotypes were assessed decades before yearly magnetic resonance images and brain autopsies were performed. Those holding more-negative age stereotypes earlier in life had significantly steeper hippocampal-volume loss and significantly greater accumulation of neurofibrillary tangles and amyloid plaques, adjusting for relevant covariates. These findings suggest a new pathway to identifying mechanisms and potential interventions related to the pathology of Alzheimer’s disease. (PsycINFO Database Record (c) 2015 APA, all rights reserved)

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

Riluzole drug can reverse key genetic changes linked to Alzheimer's disease 

Aging takes its toll on the brain, and the cells of the hippocampus--a brain region with circuitry crucial to learning and memory--are particularly vulnerable to changes that can lead to Alzheimer's disease or cognitive decline. With the hope of counteracting the changes that can lead to these two conditions, researchers at Rockefeller University and their colleagues have begun examining the effects of a drug known to affect this circuitry.

A multicenter phase 2 study showed that some patients with mild Alzheimer's disease (AD) who received deep brain stimulation of the fornix (DBS-f) experienced an increase in cerebral glucose metabolism, and some patients experienced a slowing of cognitive decline.

These positive effects were seen only in patients aged 65 years and older, not in younger patients.

Nevertheless, the findings are encouraging, said lead researcher Andres Lozano, MD, PhD, professor and chairman, Department of Neurosurgery, University of Toronto, Canada.

webmd.ads2.defineAd({id:'ads-pos-520',pos: 520}); "These findings indicate that we are headed in the right direction with our research on DBS as a treatment of Alzheimer's disease. In AD, certain areas of the brain shut down and no longer metabolize glucose to the normal level, and we hope that by stimulating the circuits in the brain that are involved, that we can restore function within the fornix and that that in turn will lead to improvement in the signs and symptoms of Alzheimer's," Dr Lozano told Medscape Medical News.

The study was published online July 18 in the Journal of Alzheimer's Disease.

TORONTO — Researchers have identified a genetic variant linked to reduced risk for Alzheimer's disease (AD), even in individuals with other elevated genetic risks for the disease. This discovery, they believe, could have important implications for a therapeutic intervention.

The research, presented here at the Alzheimer's Association International Conference (AAIC) 2016, suggests that a variant of the RAB10 gene protects against AD.

RAB10 is known to have higher expression in AD cases than in controls and has been previously linked to functional effects on amyloid secretion.

webmd.ads2.defineAd({id:'ads-pos-520',pos: 520}); This specific variant confers loss of function that improves resilience to AD and "provides us with a meaningful therapeutic target," study investigator Keoni Kauwe, PhD, associate professor, Department of Biology and Coordinator of the Bioinformatics Program, Brigham Young University, Utah, told a press briefing.

"This is not just another gene report," he said

TORONTO — A drug that inhibits tau aggregation significantly reduces disease progression in patients with mild to moderate Alzheimer's disease (AD), but only in those not already receiving standard therapy with AD medications, a new phase 3 study shows.

The study is viewed by some experts as disappointing because it failed to meet its primary endpoint of significantly reducing disease progression in all patients but as positive by others because it informs future directions for this drug.

webmd.ads2.defineAd({id:'ads-pos-520',pos: 520}); "What we have here is a potentially completely new approach to treatment that's based on the tau pathology, which is very closely linked to cognitive decline. What we have shown is that if you attack that pathway, you really do impact disease progression," said study investigator Claude M. Wischik, professor, psychiatric gerontology, University of Aberdeen, United Kingdom.

Dr Wischik is chairman of TauRX Pharmaceuticals, the company developing the new agent — leuco-methylthioninium-bis(hydromethanesulfonate) (LMTX) — a stabilized reduced form of methylthioninium.

An earlier form of the molecule was shown to be effective as monotherapy in a phase 2 trial, with the results presented in 2008 at the Alzheimer's Association International Conference and reported by Medscape Medical News at that time.

The latest findings from the phase 3 trial were presented here at the Alzheimer's Association International Conference (AAIC) 2016.

Primary Endpoint Not Met

The multicenter randomized, double-blind, placebo-controlled study included 891 patients (62% female) with probable AD who had a Mini-Mental State Examination (MMSE) score of 14 to 26, had a Clinical Dementia Rating of 1 to 2, and were younger than age 90 years.

webmd.ads2.defineAd({id:'ads-pos-420',pos: 420}); Participants were recruited at 115 sites across 16 countries in Europe, North America, Asia, and Russia and randomly assigned to one of three study groups: oral LMTX 150 mg/day, LMTX 250 mg/day, or control/placebo LMTX 8 mg/day.

Only 15% of study patients were not taking an AD medication, such as a cholinesterase inhibitor or memantine. The proportion of patients who completed the 15-month trial was 69%.

The trial's primary outcome measure was statistically significant change from baseline on standard measures of cognition and function: the Alzheimer's Disease Assessment Scale-Cognition (ADAS-Cog) and Alzheimer's Disease Cooperative Study Activities of Daily Living (ADCS-ADL) scores.

Secondary outcomes included assessment every 3 months by MRI of the lateral ventricular volume (LVV) as a disease-modifying outcome, the ADCS-Clinical Global Impression of Change (ADCS-CGIC) and MMSE.

ADAS-Cog and ADCS-ADL assessments were performed at baseline every 13 weeks thereafter. Cranial and MRI scans were performed at baseline/screening and every 13 weeks.

 https://www.researchgate.net/post/Alzheimers_disease_What_makes_it_that_complicated_to_find_a_cure

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).

Tests that measure the sense of smell may soon become common in neurologists' offices. Scientists have been finding increasing evidence that the sense of smell declines sharply in the early stages of Alzheimer's, and now a new study from the Perelman School of Medicine at the University of Pennsylvania published today in the Journal of Alzheimer's Disease confirms that administering a simple "sniff test" can enhance the accuracy of diagnosing this dreaded disease.

The sniff test also appears to be useful for diagnosing a pre-dementia condition called mild cognitive impairment (MCI), which often progresses to Alzheimer's dementia within a few years.

Neurologists have been eager to find new ways to identify people who are at high risk of Alzheimer's dementia but do not yet show any symptoms. There is a widespread consensus that Alzheimer's medications now under development may not work after dementia has set in.

"There's the exciting possibility here that a decline in the sense of smell can be used to identify people at risk years before they develop dementia," said principal investigator David R. Roalf, PhD, an assistant professor in the department of Psychiatry at Penn.

Roalf and his colleagues used a simple, commercially available test known as the Sniffin' Sticks Odor Identification Test, in which subjects must try to identify 16 different odors. They administered the sniff test, and a standard cognitive test (the Montreal Cognitive Assessment), to 728 elderly people.

The subjects had already been evaluated by doctors at Penn with an array of neurological methods, and according to expert consensus had been placed in one of three categories: "healthy older adult," "mild cognitive impairment," or "Alzheimer's dementia." Roalf and his team used the results from the cognitive test alone, or combined with the sniff test, to see how well they identified subjects in each category.

Extra-virgin olive oil (EVOO) appears to protect memory and learning ability and reduces the formation of beta amyloid (Aβ) plaques and neurofibrillary tangles in the brain — the classic hallmarks of Alzheimer's disease (AD) — new animal research shows.

The study, conducted by investigators at Temple University in Philadelphia, Pennsylvania, suggests that it is the olive oil component of the Mediterranean diet that likely promotes healthy brain aging.

"Our study is the first demonstration that EVOO can beneficially affect memory, amyloid plaques, and tau pathology, the hallmark lesions in the brain of Alzheimer's patients," lead researcher Domenico Pratico, MD, professor of pharmacology and microbiology, Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, told Medscape Medical News.

"And results are important enough to absolutely encourage people to consume greater amounts of EVOO. Given that it's been consumed for at least 2000 years, I do not anticipate any side effects," he added.

The study was published online June 21 in the Annals of Clinical and Translational Neurology.

https://www.researchgate.net/publication/281442399_Extra-Virgin_Olive_Oil_Attenuates_Amyloid-b_and_Tau_Pathologies_in_the_Brains_of_TgSwDI_Mice

Article Extra-Virgin Olive Oil Attenuates Amyloid-β and Tau Patholog...

Alzheimer prevalence is primarily reflects the Neuro Viral RNA and genome invasion of the nucleus of the inflicted neurons. Incapacitated neurons begin to compromise their kinetic capabilities whereas their local immunity against this Nucleopathology compromises.

We have had a recent experience dealing with and somewhat reverting the dementia of an 80+ old lady by rectifying the viral RNA load from the effected neuron.

http://onlinelibrary.wiley.com/doi/10.1002/acn3.431/full

Full open paper for your convenience