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Our International Press Coverage

Our discovery of ADDLs has been widely acclaimed in scientific publications, with reports in the Proceedings of the National Academy of Sciences cited more than 2,100 times. Why is this number significant?

To examine our many scientific publications, visit the publications page.

Our ADDL story has also received broad coverage in popular press and electronic media—locally, nationally and internationally. Here are some examples:

What's an ADDL

William L. Klein, a neurobiologist at the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University, is among the scientists credited with originating... the "Abeta oligomer cascade hypothesis." His claim: A smaller form of amyloid beta, or "oligomer," acts as a neurotoxin, adhering to cell receptors and jamming communication.

Click here to read the whole story.
Dr. William Klein discusses advancements in Alzheimer's research with WTTW Chicago news.

Click here to watch.
Follow Dr. Klein on a journey into Alzheimer's disease in videos produced through Neuro.RAPT.

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...recent studies reveal that proteins produced naturally in the brain could lead to new ways to treat Alzheimer's disease... The researchers showed that the type 2 diabetes drug rosiglitazone, which increases insulin sensitivity, also protects neurons from ADDLs. "Drugs designed to boost insulin signaling could provide a treatment" for the disease, says Northwestern University neurobiologist William Klein, who led the study.

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Klein, a founder of Acumen, discovered that a toxic protein called ADDL damages insulin receptors of the surface of brain cells, rendering them less responsive to the hormone. Klein and Acumen are now searching for antibodies that will counteract this toxin. "I think it's likely that if you block ADDLs, you will be able to reverse or prevent Alzheimer's..."

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...recent evidence is increasingly pointing towards much smaller, hard-to-detect soluble accumulations of A-beta as being agents of damage. Now a paper published in the 2 September issue of Proceedings of the National Academy of Sciences adds extra weight to this evidence by demonstrating that the brains of Alzheimer's disease patients contain much higher levels of soluble A-beta oligomers than control brains from unaffected individuals... association of brain-derived oligomers with neurons was investigated by incubating patient brain extracts with cultured neurons. Oligomers were found to bind in clusters to hippocampal and cortical cultures, but apparently not to cerebellar neurons, which are generally spared in Alzheimer's disease. The clustering indicated that the oligomers were behaving as ligands at discrete molecular targets...

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It only takes a small band of miscreants to stir up trouble. Small, free-floating groups of beta-amyloid molecules accumulate in brains of people with Alzheimer's disease (AD) and glom onto neurons, possibly impairing nerve signals, according to new work. The results support the idea that the intimate gatherings, rather than the crowds of beta-amyloid protein in plaques, spur the beginnings of dementia... To measure the amount of oligomers in diseased brains, neuroscientist William Klein of Northwestern University in Evanston, Illinois, and colleagues created an antibody that binds oligomers but not solitary beta-amyloid molecules... Oligomer-specific antibodies delivered to brains might destroy the structures and head off AD as well, says Klein. If such ideas gel, researchers might be on their way to preventing the molecular gangs from inciting mayhem in elderly brains.

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Alzheimer's patients may benefit from sensor research by Northwestern University chemist Richard van Duyne and neurobiologist William Klein. Klein has a theory that small proteins called amyloid beta-derived diffusible ligands (ADDLs) are key agents in Alzheimer's pathology, so he worked with researchers in van Duyne's lab to develop SPR sensors that monitor the binding of ADDLs with their antibodies.

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A quick sniff of a nasal spray sends microscopic metal particles into the brain, where they target and destroy the damaging proteins of Alzheimer's disease... Such is the promise of technology being developed by neuroscientist William Klein and nanotechnologist Vinayak Dravid of Northwestern University... The antibody created at Northwestern binds to the toxic oligomers and could one day deliver therapies to the brain or help clinicians evaluate how a patient is responding to a new medication.

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Dr. William Klein is interviewed by ABC's ScienCentral, its science affiliate.

Link to the article and listen to an excerpt of the interview, click here

"Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer's disease," William L. Klein, a researcher in Northwestern's Cognitive Neurology and Alzheimer's Disease Center and senior author of the study, said in a news release issued by the school. "Sensitivity to insulin can decline with aging, which presents a novel risk factor for Alzheimer's disease. Our results demonstrate that bolstering insulin signaling can protect neurons from harm."

Link to the article

Alzheimer's "is brain diabetes"

Treating Alzheimer's with the hormone insulin, or with drugs to boost its effect, may help patients, they claim.

The journal Proceedings of the National Academy of Sciences reports insulin could protect against damage to brain cells key to memory.

Link to the article

Insulin may be key to fighting Alzheimer's disease

Insulin, the hormone that regulates levels of sugar in the blood, may slow or prevent memory loss caused by Alzheimer’s disease, a study suggests.

Researchers examining the effects of diabetes drugs on the brain have found that the medication appears to protect cells responsible for the formation of memory.

Link to the article

Diabetes drug offers Alzheimer's hope.

Hopes were raised that diabetes drugs could be developed as treatments for Alzheimer’s disease after scientists demonstrated the beneficial effect of insulin on the brain.

A US-led research team found the hormone, released by the pancreas to help control levels of sugar in the blood, protected memory-forming parts of the brain. The study, published in the Proceedings of the National Academy of Sciences, concluded that insulin may slow or prevent the memory loss caused by toxic proteins which attack the brains of Alzheimer’s sufferers.

Link to the article

Insulin protects brain from Alzheimer's - US Study

"Our results demonstrate that bolstering insulin signaling can protect neurons from harm," William Klein of Northwestern University, whose study appears in the Proceedings of the National Academy of Sciences, said in a statement.

Klein said the findings support a new idea that Alzheimer's is a type of diabetes of the brain.

Link to the article

Insulin - Alzheimer's link found. Researchers learn that the hormone may shield the brain from toxic proteins that block new memories from being formed. (Newspaper's link to article does not work correctly at this time.)
A Northwestern University-led research team reports that insulin, by shielding memory-forming synapses from harm, may slow or prevent the damage and memory loss caused by toxic proteins in Alzheimer’s disease.

The findings, which provide additional new evidence that Alzheimer’s could be due to a novel third form of diabetes, were published online the week of February 2, 2009 by the Proceedings of the National Academy of Sciences (PNAS). To link to the press release, click here

In August [2007], a team of scientists at Northwestern University were the first to show why the brain's "memory function" fails in the face of an insulin shortage. The group's prior research had already pinpointed the culprit: toxic proteins called amyloid beta-derived diffusible ligands (ADDLs, for short), which are known to pile up in the brains of people with Alzheimer's. Scientists also knew that Alzheimer's patients' brains have lower levels of insulin and are insulin resistant. But what the Northwestern team discovered is the molecular mechanism behind that resistance: when ADDLs bind to neurons at synapses, they obliterate the receptors that are normally reserved for insulin. Without those parking spaces on the brain cells' surface, insulin has no place to connect, and memory fails.

Link to article

Highly toxic proteins trigger the first symptoms of Alzheimer’s disease … The new proteins, called Amyloid beta-Derived Diffusible Ligands ... can interfere with the process of learning and memory long before any physical damage becomes apparent, says Professor William Klein of Northwestern University. … The implications are that, if symptoms are caught at a sufficiently early stage, they might be reversed.
… (ADDLs) interfere with the process of memory consolidation …. [this] discovery may explain a longstanding mystery in Alzheimer’s research…
… discovery of ADDLs explains glaring anomalies in the conventional thinking about Alzheimer’s…
For many years, scientists thought that (plaques) might cause all the damage to neurons that is seen in AD. However, that concept has evolved considerably in the past few years. Many scientists now think that beta-amyloid clusters at an earlier stage in the plaque development process—called Ab-derived diffusible ligands, or ADDLs (also known as soluble oligomers)—may be a major culprit.
…A research team at Northwestern University has even suggested how oligomers damage neurons and cause the memory loss that features so prominently in AD… Scientists found that some oligomers attached themselves to synapses… When this happens, the synapses are not able to function properly… Unable to communicate, the neuron ultimately ceases to function and dies. As this destructive process accelerates, essential cognitive operations, such as memory formation and retrieval, are disrupted.

"Toxic proteins that interfere with memory processes essential to memory and learning have been identified.... [ADDLs] may account for the loss of memory formation in early stage and for nerve cell death and profound dementia at end stages of the disease,” says lead author William L. Klein of Northwestern University...

Insulin may protect brain against Alzheimer's

Scientists from the US and Brazil have discovered that insulin may slow or prevent the damage and loss of memory of Alzheimer's disease by blocking the action of abnormal proteins that attack brain cells, leading to the suggestion that Alzheimer's may actually be a third type of diabetes caused by weakening of insulin signalling in the brain.

Link to article


Glasgow, Scotland

“A newly discovered group of toxic proteins believed to trigger Alzheimer’s disease might be an important step towards effective treatment for the disease … Professor William Klein of Northwestern University, Illinois, who led the study, said, “Our work suggests that ADDLs may account for the loss of synaptic memory formation at the early stages of Alzheimer’s disease.”
"…previously, ADDL was found in brain tissue of Alzheimer’s sufferers, and many researchers believe it plays a role in the dementia associated with Alzheimer’s. … William Klein of Northwestern’s department of neurobiology and physiology said that the next task is to determine if ADDL can be detected circulating in the blood of Alzheimer’s patients.…"
Is Alzheimer's diabetes? Klein says the evidence is strong enough to suggest that Alzheimer's may be a type 3 diabetes. He thinks modifying current diabetes drugs for delivery to the brain could bring new treatments for Alzheimer's disease. He would also like to find ways to fight the toxic ADDLs.

Link to article

New Hope for Early Detection of Alzheimer’s: A super-sensitive test for Alzheimer’s that could identify the disease long before symptoms appear has been demonstrated on patients… The test is able to detect minute protein molecules called ADDLs which are thought to accumulate in the brain and trigger Alzheimer’s…
...scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer's disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for “amyloid ß-derived diffusible ligand.”)
A highly sensitive new test...“This is good news indeed for identifying who is at risk for Alzheimer’s and potentially for following the effectiveness of new anti-amyloid medicines …,” said (Dr. Samuel) Gandy, vice chair of the National Medical and Scientific Advisory Council of the Alzheimer’s Association

...Stephen Snyder, who directs the National Institute on Aging program studying the causes of Alzheimer’s (and was not part of the research team), said the finding [supersensitive new test] has future implications for both diagnosis and treatment...“ADDLs have been thought to be involved in diminishing aspects of cognition and this is proof of principle that they exist and can be found in spinal fluid...”

…a sensitive new test to detect proteins related to Alzheimer’s disease in spinal fluid. …the results were dramatic, and that has led medical experts to predict that a test for people who are living isn’t that far away. …
Researchers Deem Alzheimer's a Type 3 Diabetes

Link to article (pdf download)

...scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer's disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for “amyloid ß-derived diffusible ligand.”)
New Test Could Detect the Start of Alzheimer's...

Read the whole article here.
"Researchers for more than a decade thought it was big molecules, the 'amyloid fibrils,' that caused memory problems, but we think the real culprits are extremely small molecules, what we call ADDLs," said Klein, who is a member of Northwestern's Cognitive Neurology and Alzheimer's Disease Center. "Now we've shown that ADDLs are present in humans and are a clinically valid part of Alzheimer's pathology. If we can develop drugs that target and neutralize these neurotoxins, it might be possible to not only slow down memory loss, but to actually reverse it, to bring memory function back to normal."

Link to the article

Links to Other Articles

[Retired Justice] O'Connor presses for Alzheimer's research, funding CNN.com 05/14/08
Eyes on the prize: Federal Alzheimer's research effort aims to facilitate interventions Alzheimer's & Dementia 4 (2008) S37-S47
2013 Facts & Figures (National Alzheimer's Assn) National Alzheimer's Assn 2013 Report (pdf, 1.3 MB)
 

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