Find updates on the work of our researchers here, as well as news about recent advances in Alzheimer's science, funding and awareness.

Great Recognition

MassGeneral Magazine’s August issue profiles the creation of Cure Alzheimers Fund and highlights the success of our venture capital approach. The article details the innovative work being done by Dr. Tanzi, such as the Alzheimer’s Genome Project, thanks to the bold investments of Cure Alzheimer’s.

In the years when the Alzheimer’s scientific community was focused on better understanding and exploiting the four known genes implicated in the disease, Dr. Tanzi was one of few researchers advocating for finding others. By design, CAF’s founders — who had spent their careers in venture capital, banking and real estate — had established that the organization would do away with the red tape and reams of paperwork required for most grant proposals. And that modus operandi has resonated with the thousands of other donors who give to CAF.

To read the rest of the article, click here.

For a more in-depth look at the Alzheimer’s Genome Project, read MassGeneral Magazine’s article, “Unforgettable Breakthroughs in Alzheimer’s,” in the same issue.

Sharing of Data Leads to Progress on Alzheimer’s

Congratulations to the collaborators and researchers of ADNI (Alzheimer’s Disease Neuroimaging Initiative). The New York Times reports the good progress of ADNI to “find biomarkers that show the progression of Alzheimer’s disease in the human brain”.

Cure Alzheimer’s Fund is a proud contributor of this effort. Read about our funding>

Read the story in the New York Times>


We Agree.

“Bottom line: research into Alzheimer’s—its cause(s), treatment, and cure—is alarmingly urgent and terribly underfunded.”

-Marty D. from her blog The Amazing Aging Mind

There is no doubt Alzheimer’s research needs more funding. And we agree with a lot of what Marty D. wrote in her recent blog about the Alzheimer's research paradigm, funding to find a cure, and clues from our genes. Check it out:

Paradigm Lost: Alzheimer’s, beta amyloid, fund-raising, and a taboo research topic?

Spinal Fluid Tests: Who Are They Really Good For?

A NYT article about the value of using spinal fluid tests to determine the presence of Alzheimer’s disease is optimistic and hopeful but maybe too much so.

In an article published yesterday, Gina Kolata writes “Researchers are finding simple and accurate ways to detect Alzheimer’s long before there are definite symptoms. In addition to spinal fluid tests they also have new PET scans of the brain that show the telltale amyloid plaques that are a unique feature of the disease.” And “Although the latest PET scans for Alzheimer’s are not commercially available, the spinal fluid tests are. So the new results also give rise to a difficult question: Should doctors offer, or patients accept, commercially available spinal tap tests to find a disease that is yet untreatable?”

The article raises a variety of complex subjects around early diagnostics. We have blogged about "early detection" issues recently and discussed the popular media topic of “is it good to know what you have before you can cure it?” story. We have commended the research community for the development of new early detection techniques and new categories to describe pre-clinical, early signs and full involvement phases of Alzheimer’s disease FOR RESEARCH PURPOSES ONLY.

One researcher not connected with the study is quoted in the NYT article as saying: “This (spinal fluid test) is what everyone is looking for, the bull’s-eye of perfect predictive accuracy.”

Good sound bite; not an accurate interpretation of the data in the paper to which the NYT article refers.

The study in Tuesday’s Archives of Neurology includes a limited number of patients, and would have to be carried out long enough to check whether the subgroup of cognitively normal subjects who were positive for the test later get AD. Otherwise, it would be too early to use this test as a sole diagnostic for AD. At this point, the data would only warrant potential use of the spinal tap test as a "differential" diagnostic to help diagnose AD in a patient already presenting with dementia, similar to how APOE4 gene testing is used now.

The use of brain scans and other biomarkers or physical indications of the presence of AD pathology is critically important for research into how AD pathology originates, progresses and ultimately how it can be stopped; but the clinical use of these biomarkers with the general population to predict or determine the presence of Alzheimer’s is premature.

As we have written before in this blog:

“It is so easy --- and we believe wrong --- to hail a fundamental advance in research as having immediate clinical benefits when there are none at this moment. So, the net effect is to tarnish an excellent approach to useful research that will ultimately help to bring relief to patients and their families with sensational and exaggerated claims or suggested impact.”

Articles like this draw considerable media attention and can give the general public the wrong impression that there is a clear and clinically appropriate way to diagnose Alzheimer’s.  Instead, this good research should be heralded for its contribution to understanding the disease and the significant role it will play in determining the path to a cure.

This study is hopeful and optimistic but more for the research value than for immediate help for AD patients.

Read the full piece in the NYT>

ABC News agreed with us. See the segment here>

New Keys to a Cure: The Importance of Oligomers.

New Scientist published an article on how recent breakthroughs in Alzheimer’s research are questioning longstanding explanations of the disease. The article, which notes the work of two Cure Alzheimer’s Fund researchers, emphasizes an issue we have been saying for years: we need to better understand the cause, not just attack the disease symptoms.

“Thanks to a new imaging techniques, the plaques [the most common indicator of Alzheimer’s] can now be seen in the brains of living people. Not only could this allow early diagnosis, it is helping overturn the long-standing orthodoxy over the causes of Alzheimer’s, and paving the way for effective treatments.


The article notes discoveries by Sam Gandy, funded by Cure Alzheimer’s Fund, proving a correlation between oligomers and cognitive problems in mice. Dr. Rudy Tanzi, a member of the Cure Alzheimer’s Fund Research Consoritum supports Dr. Gandy’s findings.

The study is coup de grace, says Rudolph Tanzi, an Alzheimer’s researcher at Harvest Medical School and Massachusetts General Hospital. “It finally shows exactly what all the previous data were pointing to but never directly showed – we can have a brain with no plaques but still have problems.”

If interested in the full article, email



A Flash of Genius Courtesy of the Alzheimer’s Reading Room

Bob DeMarco, the editor of the Alzheimer’s Reading Room, has written a great article on Dr. Rudy Tanzi. The article introduces Dr. Tanzi’s theory on abeta’s role in the human brain, which he describes as “a sudden flash of genius.”  He also writes about his frustration with underfunded research projects and failed drug trials. We cannot agree more!

Dr. Tanzi's new hypothesis "says what we need is the equivalent of a statin for the brain so you can dial it down but not turn it off.” The it being beta amyloid, A-beta.

“It means you don’t want to hit A-beta with a sledgehammer,” Dr. Tanzi said. “It says what we need is the equivalent of a statin for the brain so you can dial it down but not turn it off.”

A sudden flash of genius? Or another bridge to no where?

It is too early to tell. I like this way of thinking outside the box. It seems to me the answer will come from outside the box.

Read more the rest of the article here.

Make sure to check the Alzheimer’s Reading Room regularly. The website is an amazing resource for news on Alzheimer’s.

Bob DeMarco is the founder and editor of the Alzheimer’s Reading Room and the caregiver for his 91-year-old mother.

Q&A from July 22, 2010 Webinar

Thank you again to the attendees of our webinar. Below are the questions we received from participants with answers from Dr. Rudy Tanzi, as well as links to additional information. We have also posted the slides of the presentation here. If you would like to download the PowerPoint file, e-mail Katie Cutler at

1.We know the disease process of Alzheimer’s starts long before the actual pathology and symptoms develop. With the growing knowledge of genes involved, wouldn't it be better to try the novel approaches in select individuals long before (say in their 50's) instead of those that have established Alzheimer's? It is disappointing (both to the researchers and the wider Alz community) to hear every time a study results are published, they come up with unsatisfactory results- Dimebon, Rember, Immunisation trials to name a few.

Yes, our goal is to use the genes to predict AD before it strikes and prevent the disease presymptomatically. I agree that it is not constructive to only focus on failed clinical trials of drugs that were not very good to begin with. Let’s focus on the next wave of therapies that have learned from these failures!

Note from Cure Alzheimer’s Fund: Check out more info on this in “Why the Drugs Don’t Work” and in “Sharing Data is Good But We Need to Better Understand Causes of the Disease”

I also wonder if other dementias - vascular/multi-infarct, mixed and frontotemporal dementias will respond to the treatments being developed for Alzheimer’s as the general consensus now appears to be mitochondrial dysfunction and neurotoxicity!

The frontal lobe dementias are based on tangle formation and tau protein abnormalities. So, drugs targeting abeta will most likely not be very helpful. This is why we also need anti-tangle drug programs.

2.What is the difference between genetic predisposition to Alzheimer's disease and familial predisposition to Alzheimer's?

The bottom line is that in familial early onset cases involving mutations in APP, presenilin 1 or presenilin 2, it is not so much predisposition as it is "causation". Any one of the ~200 mutations in these three genes guarantee Alzheimer's when inherited, usually before the patient turns 60 years old. In contrast, in late-onset AD (>60), the APOE4 gene variant increases susceptibility for AD usually between 60 and 80 (~3-fold if one parent transmits it, ~10-fold if both parents transmit it). So, this would be considered a gene variant that predisposes to AD but does not cause the disease with certainty the way the early-onset familial AD gene mutations do. Of course, you can also have familial late-onset AD and here we have found rare mutations in the ADAM10 gene that have strong effects on risk for getting the disease at about 72 years-old. In our Alzheimer's Genome Project, we have found 200 new AD gene candidates. We are currently scouring these genes to find the defects and determine whether they are causative like the early-onset familial AD gene mutations, or predisposing like the APOE 4 variant.

3.Given (as you have found) that beta amyloid has an antibiotic role in the brain, the "Alzheimer's vaccine" seemed to be the perfect Trojan Horse--wiping out beta amyloid and leaving the brain vulnerable to the agents that b-a were fighting off in the first place. You claim PBT2 takes this role of beta amyloid into account, leaving the fighting capacity of beta amyloid while removing the toxic "leftovers" of the fight. Is research also concerned about reducing the foreign cause of aggression in the brain--the agents that beta amyloid is designed to fight off? Is there perhaps an overabundance of these damaging bodies in Alzheimer's cases?

Yes, we are looking into what types of brain insults trigger the innate immune system to produce excess abeta. These insults could range from neurovascular insults, e.g. strokes or traumatic brain injury, to infections.  With regard to the latter, we are focusing on Chlamydia pneumoniae and candida albicans, given our and other’s findings.

Note from Cure Alzheimer’s Fund: For more info check out “Abeta May Have Beneficial Function as Part of the Innate Immune System

4.You said Dimebon was a failure without giving specifics of why it was a failure. From web articles, it's clear it was a failure because it did not improve memory. You also mentioned that another drug showed success (I think it was Bapi) in that it improved higher reasoning. There are plenty anecdotal accounts that Dimebon improved attention, social engagement and wit--functions that are regulated by the frontal cortex--the same area that affects higher reasoning. Why is one considered a success while the other is considered a failure for doing the same thing?

The official clinical trail results for both Dimebon and Bapi were negative in regard to cognitive improvement, which was the major primary endpoint measured for both drugs. However, in the case of Bapi, post-hoc stratification of APOE4-positive versus APOE4-negative patients showed that the latter group had some benefit. So, in the ongoing Bapi trial, I believe they included the APOE4 stratification as a primary endpoint and there could again be a positive result. The major caveat is that in the first trial and beginning of the current trial, APOE4-positive patients also suffered from more adverse side effects, including vasogenic edema (inflammation) of the brain and in some cases cerebal micro-hemorrhage. So the dose of Bapi in the ongoing trial had to be lowered for the APOE4-positive patients. We will have to wait and see if Bapi still has benefits for Cognition. Let’s hope so.

Note from Cure Alzheimer’s Fund: For more info check out “The Success Stories of Tomorrow” and “Why Don’t the Drugs Work”

From Twitter:

1.@CureAlzheimers How are Alzheimer's and Chronic Traumatic Encephalopathy different?

They are entirely different. However, any brain trauma can theoretically increase downstream risk for AD. I don’t know of any data specifically linking chronic traumatic encephalopathy to AD.

2.@CureAlzheimers Opinions on the action on the alpha-7 nAch receptor in Alzheimer’s?

These drugs have strong potential for cognitive enhancement, perhaps even beyond that of current drugs on the market and maybe even working well in concert with each other. However, they would most likely just be treating the symptoms rather than the actual disease. We would certainly welcome their appearance!

Thank you again for attending our webinar! To stay up-to-date on our work, follow us on twitter at or like us on facebook at

Slides from the Webinar

Thank you to those who attended our Webinar on July 22 titled “Working Toward a Cure for Alzheimer’s: Clues from our Genes”. Below are the slides from the event. Video clips addressing key components of the presentation and blog posts responding to questions from the webinar will be posted shortly.

Click each slide to advance.

Brain Scan Diagnostics for early detection of Alzheimer’s --- a good idea?

There is debate about this.  A panel of leading Alzheimer’s researchers has recommended new guidelines for earlier diagnosis of Alzheimer’s Disease (AD), including the use of brain imaging.  While most commentators have hailed this news, a few have raised concerns. One of the clearer expositions of this was a Forbes online blog by Robert Langreth on July 15 entitled “A Scary Idea: Pre-emptive Brain Scans for Alzheimer’s.”

Langreth hypothesizes this diagnostic report:
“You feel fine and have no symptoms, but your brain is slowly rotting away. And there is nothing we can do about it.” Maybe he should have added “now”.

What is behind all this, and is this proposal really useful for patients and research?

"CAF's Sam Gandy delivers "Hot Topics" session at International Conference on Alzheimer's Disease (ICAD)"

At ICAD 2010 in Hawaii Dr. Sam Gandy of Cure Alzheimer's Research Consortium presented the results of a study showing a new class of biomarkers that can stick to protein structures in the body and emit colors reflecting the different shapes or forms of the proteins. They are called luminescent conjugated oligothiophenes (LCOs) or luminescent conjugated polymers (LCPs). Among other uses, they are currently being employed in test tubes, animal models and autopsied Alzheimer’s brains to study the structure of protein deposits caused by the disease. The new markers bind to the two well-established hallmarks of Alzheimer’s – beta amyloid plaques and tau tangles – and glow different colors depending on which forms of the deposits they “stick” to (e.g., plaques often “glow” orange, while tangles glow yellowish green).