Common antidepressant may halt plaque growth associated with Alzheimer’s

Common antidepressant may halt plaque growth associated with Alzheimer’s

By Amanda Woerner
·Published May 15, 2014·


One hemisphere of a healthy brain (L) is pictured next to one hemisphere of a brain of a person suffering from Alzheimer disease, at the Belle Idee University Hospital near Geneva March 14, 2011. (REUTERS/Denis Balibouse)

A commonly used medication could hold the key to treating or preventing Alzheimer’s disease.

New research published in the journal Science Translational Medicine reveals that the frequently prescribed antidepressant citalopram, also known as Celexa, could play a role in halting the progression of the brain-wasting disease.

Antidepressants like citalopram offer hope by targeting the brain’s amyloid beta proteins, which seem to be responsible for triggering the plaque build-up associated with the decline of memory and cognitive function in Alzheimer’s patients.

“The way the Alzheimer’s field is going is [we are] trying to find the initial insult in Alzheimer’s disease,” study author John Cirrito, assistant professor of neurology at the Washington University School of Medicine, told “We think it is the build-up of this amyloid beta peptide, and once it builds up, a lot of things go wrong.”

Amyloid beta proteins are produced by normal brain activity, but in Alzheimer’s patients, levels of this protein increase abnormally, clumping together to form plaques.

Previous research has shown that serotonin, a brain chemical thought to influence mood, seems to reduce amyloid beta production in the brain. In fact, an earlier study demonstrated that people with a history of antidepressant use had less amyloid plaques in their brains than those who never used antidepressants.

A popular type of antidepressant known as selective serotonin reuptake inhibitors (SSRIs) can influence serotonin levels, so the researchers were interested in testing its effects on mice and human models. Using mice genetically engineered to develop Alzheimer’s disease, the researchers discovered that the SSRI citalopram was able to completely stop the growth of brain plaques in the study group.

“SSRIs, by lowering a-beta levels 25 percent, were able to completely block that [plaque] growth,” Cirrito said. “The plaques never got smaller, and we couldn’t reverse the plaque [that was already there], but we could prevent it from growing.”

The researchers also tested citalopram in a group of cognitively healthy young adults. They discovered that after receiving a single dose of the antidepressant, the participants saw a 37 percent reduction of amyloid beta levels in their cerebrospinal fluid.

Currently, Cirrito said amyloid beta has no “known function” in the human body, and decreasing levels of the protein in humans doesn’t seem to have any ill effects on health. However, he noted that much research needs to be done before SSRIs can be proven effective at treating or preventing Alzheimer’s in humans.

“The SSRIs in this study were all given to healthy young people not at risk for Alzheimer’s,” Cirrito said. “We don’t know if the same thing will happen in people older, and not at risk for Alzheimer’s, and have no idea if it affects cognition,” Cirrito said.

Furthermore, he cautioned people against preemptively taking SSRIs in hopes of fending off or treating Alzheimer’s disease.

“There are certainly side effects [of SSRIs] that if they don’t need to be taken, it’s not a good idea to be on them until we know they can have an effect on Alzheimer’s, it’s premature to take them as a preventative measure,” Cirrito noted. “We’ve cured a mouse of a lot of different diseases, including Alzheimer’s disease many times, and those things haven’t panned out in people yet.”

Next, Cirrito and his team hope to move forward to study how SSRIs act on the brain to lower amyloid beta levels – and to continue to study the effects of SSRIs on different human populations.

“On the human side, we’re doing a similar study to what we just completed but in people [who are] older and at risk for Alzheimer’s, to see if we can affect a-beta in those people or not,” Cirrito said. “If not, then the utility of this for people with Alzheimer’s would go down dramatically.”

New Alzheimer’s discovery

New Alzheimer’s discovery could hold key to preventative treatments for high-risk patients

By Amanda Woerner

Published October 22, 2013
  • Head X-ray istock.JPG

For years, people with a family history of Alzheimer’s disease have shied away from genetic testing, which could reveal that they carry the ApoE4 protein – a genetic risk factor associated with a 10-fold higher chance of developing the incurable neurodegenerative condition.

However, new research has highlighted a potential pathway for early intervention methods that could help those at a high risk for Alzheimer’s, making genetic screening for the disease as important as cholesterol tests are to preventing heart disease.

Researchers from The Buck Institute for Research on Aging, an independent research association based in Novato, Calif., have long been interested in discovering why ApoE4 is associated with such a high risk for Alzheimer’s disease.  

“Why is this the dominant risk factor?” study author Dr. Dale Bredesen, founding CEO of the Buck Institute, told “Though people have known this for 20 years, it’s never been clear what it is that ApoE4 does to confer such risk.”

Prior research had focused on the discovery that ApoE4 appears to affect the clearance of amyloid-beta (A-beta), a plaque that builds up in the brains of patients with Alzheimer’s disease. However, Bredesen and his colleagues weren’t convinced that this finding told the whole story of why ApoE4 causes Alzheimer’s.

“Treating that hasn’t worked very well,” Bredesen said. “There’s an emerging feeling, which we believe, that this is more than just about A-beta.”

In a study published in The Proceedings of the National Academy of Sciences, Bredesen and his colleagues analyzed ApoE4 cell cultures and discovered that ApoE4 was also associated with a dramatic reduction in SirT1 – a protein associated with anti-inflammation, anti-aging and longevity.

Bredesen said that as SirT1 decreases, it affects a certain protein crucial to the storage or loss of memories – the amyloid precursor protein (APP).

“You have a molecule called the APP, present in neurons and most cells in your body, and at all times this APP is getting cleaved,” Bredesen said. “It turns out there are two alternative patterns. So it is a little bit like how the government can go on shutdown or active. APP can go in the direction of memory or forgetting.”

In Alzheimer’s, Bredesen says people are on the ‘wrong side’ of this process – causing them to forget rather than retain memories.

However, by maintaining SirT1 levels, researchers believe they may be able to prevent these proteins from going awry. As a result of their discovery, Bredesen and his colleagues attempted to identify drugs that might be able to maintain levels of SirT1 in ApoE4 cell cultures. So far, they have successfully identified four drugs that seem to be effective – though they have yet to test their findings in humans.

“It gives us a leg up on saying, ‘Okay, we can begin to look at how to treat people with ApoE4 even when they’re young to make sure they never get Alzheimer’s, by affecting that link between ApoE4and Alzheimer’s,’” Bredesen said.

Furthermore, Bredesen and his colleagues also performed experiments in which they successfully reinserted SirT1 proteins back into cells already affected by ApoE4. By doing this, they were able to correct the abnormalities present in the cell and return it to a healthy state. This led Bredesen and his colleagues to speculate that treatment might be possible even for those already entering the early stages of Alzheimer’s.

“Most people today don’t want to know if they have ApoE4 because what can they do about it? This could change the landscape where we say everyone should know, just like with high cholesterol or high blood pressure, because you can do something about it,” Bredesen said.

Women’s height linked to cancer risk, study shows

Women’s height linked to cancer risk, study shows

By Amanda Woerner

Published July 25, 2013
  • cancer_cells.jpg

    Cancer cells. (iStock)

Height may be a disadvantage for some women when it comes to their risk for developing cancer. A new study published in the journal Cancer Epidemiology, Biomarker’s and Prevention indicates that taller women are at a greater risk for contracting some forms of the disease.

Furthermore, researchers said their findings held strong even when controlling for numerous other factors linked to cancer, such as body mass index (BMI).

“We didn’t find much difference in heavy or lighter women, so it’s a pretty consistent association right across the spectrum,” senior study author Dr. Thomas Rohan, chair and professor of epidemiology and population health at Albert Einstein College of Medicine in New York City, told

In a 12-year study of 20,928 postmenopausal women, researchers noted that height was linked to breast, colon, endometrium, kidney, ovary, rectum, and thyroid cancers – as well as multiple myeloma and melanoma.

The taller the women were, the higher their cancer risk. Each 3.95 inch increase in height was associated with a 13 percent increased risk for developing any type of cancer, when researchers compared the heights of all women in the study. For example, a woman who was 5 feet 10 inches tall would have a 13 percent higher risk for cancer than a woman who was approximately 5 feet 6 inches tall.

Furthermore, some cancers were more strongly associated with height than others. For cancers of the kidney, rectum, thyroid and blood, women experienced a 23 percent to 29 percent increased risk with each incremental gain in height.

While researchers can’t say exactly why the link exists, they have a few theories.

“There are many genetic determinants of height, and some may also be related to cancer risks,” Rohan said.

Another potential explanation may be related to environmental factors, such as childhood nutrition.  Increased energy intake during childhood is thought to influence adult height and may also impact certain systems in the body, according to Rohan.

“The intake may influence height, which somehow is influencing cancer risk,” Rohan said. “It may have an effect on hormones, which…may influence cancer risk.”

However, Rohan points out that many additional factors throughout adolescence and young adulthood could also be influencing women’s risk for cancer – and that a true explanation for this phenomenon remains unknown.

Despite their findings, Rohan and his fellow researchers hope that taller women don’t lose sleep over the matter. Instead, he hopes researchers will continue to explore the link between height and cancer, as they search for some of the underlying biological mechanisms that may be responsible for the correlation.

“The goal of this study was not to make clinical recommendations,” Rohan said. “From my perspective, this is an interesting observation. But there’s enough for people to worry about without worrying about how tall they are.”

Read more:

Young stroke victim recovers with help from new electrical stimulation technology

Young stroke victim recovers with help from new electrical stimulation technology


Published May 20, 2013

  • Wes CHoP ICU.jpg

    After his stroke, Wes (pictured here) was treated in the intensive care unit of The Children’s Hospital of Philadelphia. ((Schlauch family))

  • Wes Hill Formal.jpg

    Wes, using his cane, on his way to high school prom. ((Schlauch family))

  • Wes in Hill Game.jpg

    SONY DSC ((Schlauch family))

  • Wes Schlauch_Hill School Graduation.jpg
    (Schlauch family)
When Wes Schlauch, of Breinigsville, PA, was 16 years old, he suffered a stroke that paralyzed the entire right side of his body. Miraculously, three years later, Wes is not only walking and talking – he’s even sending text messages, attending college and going on fishing trips with friends.
Wes’ positive attitude, devotion to rehabilitation and strong support system has had much to do with his success. But Wes has also benefitted tremendously from a cutting-edge technology that is revolutionizing therapies for patients suffering from brain injuries and neurodegenerative diseases: a new treatment known as functional electrical stimulation (FES).FES has been pioneered by companies like Bioness Inc., based in Valencia, CA., which created the devices that Wes uses. The devices – which Wes wears on both his right hand and leg – use electricity to stimulate the damaged portions of his brain and the neural connections between the brain and muscles.

“The idea is that by using the electrical stimulation to make the muscle fire, his brain will retrain and relearn, and his muscles will fire more automatically without it in the long term,” Jolene Hammer, a physical therapist at Lehigh Valley Hospital in Bethlehem, PA., who works with Wes, told

FOUR IN 100,000
Strokes are incredibly rare among children and teenagers like Wes.

“From after the newborn period through age 18, the incidence (of stroke) that we estimate is about four in 100,000 children per year,” Dr. Rebecca Ichord, director of the pediatric stroke program at The Children’s Hospital of Philadelphia, who treated Wes, told

According to Ichord, Wes’ stroke was likely triggered after he experienced whiplash while playing hockey. Doctors believe that one of the arteries in Wes’ neck twisted and dissected, causing the walls of the artery to separate. This caused a blockage in Wes’ blood flow that led to the formation of a clot – resulting in a stroke.

Wes’ stroke was particularly devastating because it occurred in his baseline artery, which facilitates blood flow to critical parts of the brain.

“(His) was one of the most severe types of strokes; when you block the baseline artery, you block critical parts of brain systems that control all elements of function,” Ichord said. “The mortality is relatively higher than in other types of stroke and long term handicap can be devastating.”

Luckily, Wes was able to receive a clot-dissolving therapy within eight hours of his stroke, which restored blood flow to the injured part of his brain. However, Wes still had a long journey ahead of him. The right side of Wes’ body was paralyzed – a condition called hemiparesis.

“I remember lying in the hospital bed and looking up at the ceiling, because that’s all I could do,” Wes told “My respiratory therapist told me to visualize myself getting better so I just visualized myself getting out of that situation.”

Eventually, Wes stabilized and was moved to a rehabilitation facility where he had to relearn basic daily tasks, like dressing himself and eating – all the while confined to a wheelchair.


Fortunately, Wes didn’t stay in his wheelchair for long.  He soon progressed to a walker and then to a cane. As Wes regained his strength, he was able to begin FES treatments, with the help of his rehabilitation team.

To regain the use of his right hand, Wes eventually began using the Bioness NESS H200® Hand Rehabilitation System – an external device that Wes wears on his hand and arm.

“That’s helped me be able to be more dexterous with my movements and has overall helped my hand big time,” Wes said. “It used to be that my hand was in a fist, and I wasn’t able to use it at all. I got the H200 device and I was able to use my hand nicely.”

“I’ve even been known to text with my right hand,” Wes added.

Later, Wes progressed to the NESS L300™ Foot Drop System, which allowed his foot to move more freely.

“As he’s been using it, I see that he’s now able to start to actively move those muscles without it that he wasn’t before…Now, he can lift his foot and be aware of it and pull it up on his own,” Hammer said. “He has gotten to be able to lift his toe up and to be able to activate his hamstring.

Just last week, Wes took home a new device – the L300 Plus – which he will wear on his thigh to stimulate his hamstring. Wes will use this in conjunction with the L300 in order to gain further control over his leg, bolstering his ability to walk and even maneuver stairs.

Though Wes gets fatigued easily (especially when using the devices), he is building up his tolerance and strength, and he eventually hopes to be able to wear both the L300 and L300 Plus for full days.

“It’s helped my walking a ton and being able to walk around the community is a lot better for me as opposed to just being in a wheelchair like I was before. Now I’m on a cane. It’s helped me a lot,” Wes said.

Wes’ doctors hope that technology like the Bioness devices will eventually help repair the damaged parts of Wes’ brain to some extent.

“I think it’s a cutting edge way to start to work on retraining the muscle and hopefully to play into neuroplasticity, to activate the brain to make new connections and to activate these muscles,” Hammer said.

Wes continues to make extraordinary advances in his treatment and personal life – even making the dean’s list at college.

“His speech is also a little affected, but he can still communicate,” Ichord said. “And his cognitive learning abilities, personality and sense of humor (were) all preserved; the thinking part is doing well and was never directly affected.”

Wes credits his experience as a hockey player for giving him his strong work ethic.

“I work hard, I always did – back from when I was 16 on. I worked as hard as I could and…I really want to get back on the ice. That’s my main motivating factor,” Wes said.

Wes continues to impress his physical therapists and doctors every day, and Hammer said she has high hopes for Wes’ future progress.

“I’ve been a therapist for a long time and he’s an extraordinary young man – one of the most motivated people I’ve met. If every patient worked as hard as him, I’d be out of a job,” Hammer said.

Read more: