National Dementia Association Launches Awareness Month

(NewsWise) In an effort to drive awareness of a common but little known dementia, Lewy body dementia (LBD) families are hosting events nationwide to help raise support for those affected by the disease. Greater public awareness is desperately needed, as LBD is the most misdiagnosed form of dementia.

Lewy Who?


LBD is the second most common form of dementia, afflicting 1.4 million Americans. Symptoms resemble Alzheimer’s and Parkinson’s disease, but treatment may not. Correct early diagnosis can protect patients from receiving meds and treatments that could make symptoms worse.

LBD is the most misdiagnosed form of dementia. Most people are not diagnosed until at moderate or severe states. It takes on average over 18 months and three doctor visits to receive a correct diagnosis. That’s a missed opportunity that can leave people and their families unprepared and vulnerable.

The timing of these events aligns with the October National Lewy Body Dementia Awareness Month, driven by the Lewy Body Dementia Association (LBDA). Events are being organized across the country to help increase awareness. Educating the public about LBD symptoms to report to the doctor is a vital step in decreasing the time it takes to receive a diagnosis.

LBDA encourages people and organizations to host or attend local events to learn more about the disease, how it impacts those diagnosed, their caregivers and families. Participants will better be able to answer the question, “Lewy Who?” and help spread awareness of this devastating disease.

Proceeds raised will be donated to LBDA, the only organization in the United States that provides comprehensive education and support for the 1.4 million people and the families affected by LBD.

“Hosting or attending Awareness Movement events across the country during the month of October will help not only to spread the word about LBD but also to increase the base of support for LBD families,” says Michael Koehler, president of Lewy Body Dementia Association. “It takes a united front to make an impact and to provide vital information and outreach to those affected by this condition.”

To learn how you can help spread awareness, or find an event near you, visit

About Lewy Body Dementia Association

The Lewy Body Dementia Association (LBDA) is a 501(c)(3) national nonprofit health organization dedicated to raising awareness of Lewy body dementia (LBD), promoting scientific advances, and supporting people with LBD, their families and caregivers. LBD, a complex disease that can present with a range of physical, cognitive, and behavioral symptoms, is a “family disease.”

It dramatically affects not only the person diagnosed but also the primary caregiver. LBDA supports all those affected by Lewy body dementia through outreach, education and research. To learn more about LBD and LBDA, please visit



Memory Concerns Presage Cognitive Decline and Aβ Pathology

(AlzForum) A perceived slip in memory could signal future cognitive decline, suggests a paper in the October 7 Neurology. Researchers led by Richard Kryscio, University of Kentucky, Lexington, found that ostensibly normal volunteers who reported a subjective memory complaint were nearly three times likelier than non-complainers to meet criteria for mild cognitive impairment (MCI) or dementia over the next 10 years.

They also had more amyloid in their brains. Alzforum reported on these findings when they were presented at a conference last year (see Jul 2013 conference story). The study was covered by CBSCNN, and The Los Angeles Times.

“This is one of the few studies that chronicles the transition from subjective memory complaint to impairment,” said Frank Jessen, German Center for Neurodegenerative Diseases, Bonn.

Subjective cognitive decline, also known as subjective memory complaint (SMC), was recently defined as “self-experienced persistent decline in cognitive capacity in comparison with a previously normal status and unrelated to an acute event” (see Jessen et al., 2014). This can be rooted in depression, lack of vitamin B12, certain medications, or normal aging processes, but it may also reflect early Alzheimer’s disease.

“Not everyone who complains develops an impairment,” Kryscio told Alzforum.

His group wanted to determine how many people progress from SMC to MCI or dementia, what they term an “impaired state” in this study, and how fast, and how that correlated with AD pathology.

In 1989, Kryscio and colleagues began studying 531 cognitively healthy people, average age 73, from the Biologically Resilient Adults in Neurological Studies (BRAiNS) cohort, a longitudinal observational study and brain donation program at the University of Kentucky.

Yearly psychological tests assessed memory, language, executive and visuospatial function, and whether the subject had progressed to MCI or dementia. Before each round of testing, researchers asked the participants if they had noticed any change in memory since their last visit. If they answered yes, they were tagged as reporting an SMC. They donated their brain after death to be examined for signs of plaques or neurofibrillary tangles, the two hallmarks of Alzheimer’s pathology.

Of 296 people who declared an SMC, 114 progressed to MCI or dementia over about nine or 12 years, respectively. Having an ApoE4 allele doubled a person’s risk of becoming impaired, and smokers progressed to MCI almost three years faster. Interestingly, women on hormone replacement therapy progressed more slowly.

Research conflicts about whether supplemental estrogen protects from dementia or enhances risk (see Nov 2011 news story). Because the time to impairment varied depending on environmental factors, the study suggests that interventions could target the disease during this period, the authors wrote. Jessen agreed. “I predict these will be the subjects we treat in the future,” he told Alzforum.

Almost half of the original participants have come to autopsy. About a quarter of those who died without SMC or impairment had moderate to severe Aβ pathology in the brain, as did roughly a third of those who declared an SMC but did not progress to MCI or dementia. Of the 50 with SMC who became impaired, three-quarters accumulated abundant plaques and tangles. That amyloid built up in the SMC group but neurofibrillary tangles only appeared at impairment suggests that amyloid has an effect on cognition, said Jessen.

The researchers have not scanned the living volunteers to see if they have brain amyloid because PET amyloid ligands were not available when this study started, said Kryscio. He has no plans to add it at this point.

The study agrees with several others that use postmortem evidence or PET to correlate SMC with elevated amyloid build-up (see Barnes et al., 2006Perrotin et al., 2012Amariglio et al., 2012). It also jibes with a recent meta-analysis that found older people with SMC are twice as likely to develop dementia as people with no complaint (see Mitchell et al., 2014).

Researchers have yet to agree on a standard way to measure SMC, said Ron Petersen, Mayo Clinic, Rochester, Minnesota. The single survey question used in the Kryscio study captures some element of subjective concern but is quite basic, he said. Predicting whether an SMC could lead to dementia may depend on the type of memory change, suggested one study (see Amariglio et al., 2011).

Results imply that getting lost in familiar places or being unable to follow a group conversation predict future cognitive decline better than forgetting things from one second to the next.



Jealous, Moody Women and Alzheimer’s Risk

(WebMD) Middle-aged women with a neurotic personality style and prolonged stress may have a heightened risk of developing Alzheimer’s disease, new research suggests.

Tracking 800 women over nearly four decades, Swedish scientists found that those who were most anxious, jealous and moody — which they defined as neurotic — and experienced long-standing stress had double the risk of developing Alzheimer’s compared to women scoring lowest in these traits.

“No other study has shown that [one style of] midlife personality increased the risk of Alzheimer’s disease over a period of nearly 40 years,” said study author Lena Johansson, a researcher at University of Gothenburg.

Outside experts cautioned, however, that the study results don’t prove that neuroticism triggers Alzheimer’s, but they do suggest an association between the two.

The study is published online Oct. 1 in the journal Neurology.

The most common type of dementia, Alzheimer’s disease causes profound memory loss and impairments in language, focus, judgment and visual perception, according to the Alzheimer’s Association. About 5.2 million Americans have been diagnosed with Alzheimer’s, which is progressive, incurable and ultimately fatal.

Johansson said she believes the results would also be true for men. But study data — pulled from research that began in the 1960s — happened to include only women in an era when few medical studies focused on females.

In the new study, participants with an average age of 46 were tracked for 38 years and given memory tests and personality tests measuring their levels of neuroticism and extraversion (defined as being outgoing) and introversion (defined as reserved or shy).

Study authors defined neuroticism as being easily distressed and exhibiting personality traits such as anxiety, jealousy or moodiness. People with this personality style are more likely, they said, to express guilt, anger, envy, worry and depression.

The women were also asked if they had experienced any period of prolonged stress lasting one month or longer and to rate their stress on a scale from zero to five, which represented constant stress during the previous five years. Stress responses included nervousness, sleep disturbances, fearfulness, irritability and tension.

Being introverted or extroverted alone didn’t seem to affect dementia risk, but women who were both easily distressed and withdrawn (introverted) had the highest risk of Alzheimer’s among all women analyzed. One-quarter of them developed the disease, compared to only 13 percent of those considered outgoing (extroverted) and not easily distressed.

“We know genetics drives personality and disease itself, but there’s very little understanding of how personality drives disease,” said Dean Hartley, director of science initiatives for the Alzheimer’s Association, who was not involved in the research. “We need more data.”

Just how might personality influence the risk for dementia? By influencing a person’s behavior, lifestyle or stress reactions, all of which affect overall health, Johansson said. Also, prior research has indicated that neuroticism and stress are associated with changes in the hippocampus, a brain structure affected early in Alzheimer’s disease.

Hartley said the new research was limited in its ability to measure participants’ actual stress levels, since it did so by asking them a single question about stress every five years instead of measuring specific biochemical responses to stress.

“Future studies should examine . . . whether this [neurotic] group responds well to interventions,” Johansson said. “It remains to be seen whether neuroticism could be modified by medical treatment or through lifestyle changes.”



Protein that Causes Frontotemporal Dementia also Implicated in Alzheimer’s Disease

(Gladstone Institutes) Researchers at the Gladstone Institutes have shown that low levels of the protein progranulin in the brain can increase the formation of amyloid-beta plaques (a hallmark of Alzheimer’s disease), cause neuroinflammation, and worsen memory deficits in a mouse model of this condition. Conversely, by using a gene therapy approach to elevate progranulin levels, scientists were able to prevent these abnormalities and block cell death in this model.

Progranulin deficiency is known to cause another neurodegenerative disorder, frontotemporal dementia (FTD), but its role in Alzheimer’s disease was previously unclear. Although the two conditions are similar, FTD is associated with greater injury to cells in the frontal cortex, causing behavioral and personality changes, whereas Alzheimer’s disease predominantly affects memory centers in the hippocampus and temporal cortex.

Earlier research showed that progranulin levels were elevated near plaques in the brains of patients with Alzheimer’s disease, but it was unknown whether this effect counteracted or exacerbated neurodegeneration. The new evidence, published today in Nature Medicine, shows that a reduction of the protein can severely aggravate symptoms, while increases in progranulin may be the brain’s attempt at fighting the inflammation associated with the disease.


According to first author S. Sakura Minami, PhD, a postdoctoral fellow at the Gladstone Institutes, “This is the first study providing evidence for a protective role of progranulin in Alzheimer’s disease. Prior research had shown a link between Alzheimer’s and progranulin, but the nature of the association was unclear. Our study demonstrates that progranulin deficiency may promote Alzheimer’s disease, with decreased levels rendering the brain vulnerable to amyloid-beta toxicity.”

In the study, the researchers manipulated several different mouse models of Alzheimer’s disease, genetically raising or lowering their progranulin levels. Reducing progranulin markedly increased amyloid-beta plaque deposits in the brain as well as memory impairments. Progranulin deficiency also triggered an over-active immune response in the brain, which can contribute to neurological disorders. In contrast, increasing progranulin levels via gene therapy effectively lowered amyloid beta levels, protecting against cell toxicity and reversing the cognitive deficits typically seen in these Alzheimer’s models.

These effects appear to be linked to progranulin’s involvement in phagocytosis, a type of cellular house-keeping whereby cells “eat” other dead cells, debris, and large molecules. Low levels of progranulin can impair this process, leading to increased amyloid beta deposition. Conversely, increasing progranulin levels enhanced phagocytosis, decreasing the plaque load and preventing neuron death.

“The profound protective effects of progranulin against both amyloid-beta deposits and cell toxicity have important therapeutic implications,” said senior author Li Gan, PhD, an associate investigator at Gladstone and associate professor of neurology at the University of California, San Francisco. “The next step will be to develop progranulin-enhancing approaches that can be used as potential novel treatments, not only for frontotemporal dementia, but also for Alzheimer’s disease.”

Other authors on the study include Sang-Won Min, Grietje Krabbe, Chao Wang, Yungui Zhou, Rustam Asgarov, Yaqiao Li, Lauren Martens, Lisa Elia, Michael Ward, Lennart Mucke, and Robert Farese. Funding for the research was provided by the Consortium for Frontotemporal Dementia, National Institutes of Health, and the S. D. Bechtel, Jr. Foundation.

About the Gladstone Institutes

To ensure our work does the greatest good, the Gladstone Institutes focus on conditions with profound medical, economic, and social impact – unsolved diseases of the brain, the heart, and the immune system. Affiliated with the University of California, San Francisco, Gladstone is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease.



Dementia Risk on the Decline in Developed Countries

(Alzheimer’s Prevention Registry) A headline that includes the words “dementia” and “decline” is good news. However, the news out of Copenhagen—site of the Alzheimer’s Association International Conference 2014 (July 12-17)—received a mixed reception. While researchers presented data showing the incidence of dementia has declined gradually in the U.S. and Europe, they also stated its prevalence may be underreported in developing countries, like Colombia and large regions of Africa and Asia. In total, Alzheimer’s Disease International (ADI)estimates that in 2013 there were approximately 44 million people living with dementia throughout the world.

What’s behind the decline in the prevalence of dementia in the U.S. and other developed countries? According to the researchers, more aggressive treatment of heart disease, hypertension and high cholesterol may be contributing to better brain health and a decline in the number of new cases of Alzheimer’s disease and dementia in certain countries and regions of the world. This improved disease management, rather than any change in the pathology of Alzheimer’s disease or dementia, is believed to contribute to their lower rates in certain parts of the world.

“Generally speaking, cardiovascular risk factors tend to also increase one’s risk of developing dementia,” said Gabrielle Strobel, executive editor of Alzforum. “This is particularly true of hypertension during midlife. Left untreated, elevated blood pressure is thought over time to damage the lining of the small blood vessels in the brain.”

A 20-year study, released August 4 in The Journal of the American Medical Association (JAMA) Neurology, supports the link between high blood pressure and increased risk for dementia. Researchers found that people who began the study with high blood pressure performed worse on cognitive tests at the end of the study than people with normal blood pressure or people whose high blood pressure was treated.

Researchers have yet to draw a definite line between lifestyle and dementia. However, they believe that exercise, a healthy diet, and weight control—all of which can stave off diabetes and improve cardiovascular health—may also protect against dementia.

“It is absolutely worth making healthy lifestyle changes to improve one’s overall health,” Strobel said. “But there is never a guarantee that these changes will avoid dementia in any given person.”



Promising Alzheimer’s Treatment Being Tested by Neuro Company and U.S. Research University

(NeuroEM Therapeutics) A Phoenix-based medical device R&D company, announced today that it has begun a study with a premiere research university (University of South Florida) to test its Transcranial Electromagnetic Treatment (TEMT) in aged primates.

“All attempts to treat Alzheimer’s through drugs have thus far been very disappointing, so our medical device represents a new therapeutic direction,” said Dr. Gary Arendash, President and CEO of NeuroEM Therapeutics.

“Aged primates (Rhesus monkeys) develop the same abnormal amyloid deposits in their brains as Alzheimer’s patients and they also become cognitively impaired during aging,” Dr. Arendash indicated.

He and his colleagues had previously found that their patent-pending TEMT technology reverses both Alzheimer’s brain pathology and severe memory impairment in aged Alzheimer’s mice.  These mice had been genetically modified to produce human amyloid deposits, which are thought to cause Alzheimer’s disease.

However, primates are much closer to humans in brain structure and function.  Moreover, they spontaneously develop amyloid plaques in their brains during aging identical to those in human AD patients.  A therapeutic that is found to be beneficial to these aged primates is likely to provide the same benefits in Alzheimer’s patients.

For the study, researchers at NeuroEM’s collaborating university are administering TEMT to aged primates over several months while monitoring cognitive performance and brain function.  TEMT is completely non-invasive, so subjects will not even be aware of it.

“The primates being used in this study are all substantially aged, which affords us a unique opportunity to get important, Alzheimer’s-related data during the treatment period,” stated Dr. Arendash.  Dr. Chuanhai Cao at the University of South Florida, who helped develop TEMT technology with Dr. Arendash, is performing the study’s biochemical analyses.

TEMT has two ways that it directly attacks the Alzheimer’s disease process.  First, it disaggregates amyloid plaques both inside and outside of brain cells.  Secondly, it increases brain metabolism by enhancing mitochondrial function.  Both of these mechanisms are unique to TEMT in that no drug being clinical tested against Alzheimer’s offers them.

“If our collaborative primate study is successful, clinical trials with TEMT administration to Alzheimer’s patients could begin by next summer,” indicated Dr. Arendash.  “NeuroEM Therapeutics has a projected time line to commercialize its medical device of under 5 years, which is much faster than for an Alzheimer’s drug,” said Dr. Arendash.

NeuroEM’s head device for Alzheimer’s treatment is designed to be self-contained for comfortable in-home treatment, allowing complete mobility.  The company has several pending patents for use of TEMT against neurodegenerative diseases.  Numerous studies have shown the technology to be safe for humans.  The head device would only be available through neurologists and other health professions qualified to diagnose Alzheimer’s Disease.

Alzheimer’s affects over 5 million Americans, with the U.S. market being $4-10 billion annually for an effective therapeutic. More information about NeuroEM Therapeutics and TEMT technology can be found at the company’s website (



Scientists Create New ‘Designer Proteins’ in Fight Against Alzheimer’s and Cancer

(University of Leicester) Chemists at the University of Leicester have reported a breakthrough in techniques to develop new drugs in the fight against diseases such as cancer and Alzheimer’s.

The team has developed an innovative process allowing them to generate a particular type of synthetic amino acid – and a particular type of designer protein – that has not been done before.

The advance is announced by the Jamieson Research Group in the Department of Chemistry at the University of Leicester.  Their work, funded by the Engineering and Physical Sciences Research Council (EPSRC), is published in the Royal Society of Chemistry journal Organic and Biomolecular Chemistry.

Dr Andrew Jamieson, lead scientist, said:

“We are very proud of this research, it has taken several years of hard work to master the chemistry techniques to create these new building blocks but now that we have conquered it we have access to new building blocks that people have only ever dreamed of before!”

Amino acids are Mother Nature’s building blocks. They are used to make all proteins and so are essential for life, however Mother Nature only uses twenty of these building blocks. The Leicester research involves the chemical synthesis of unnatural amino acids that can be used to make unnatural mini-proteins with new 3D structures and importantly new functions.

Dr Jamieson said:

“We are particular interested in using our new building blocks to develop innovative new protein drugs for the treatment of cancer and Alzheimer’s disease.

“Unnatural amino acids, the building blocks, are described as chiral, meaning they have “handedness”. A robust synthesis to selectively produce molecules with a particular handedness has not previously been reported.

“Our new practical method allows us to selectively synthesise only the “right handed molecules”.

“This new research is important because it has uncovered a new, easier and quicker way to make these building blocks which can be used to make new drugs.  We now have access to new building blocks to develop innovative new protein drugs for the treatment of disease.

“We are actively using these building blocks to develop new treatments for cancer and Alzheimer’s disease. We have also had a summer student use the building blocks to synthesise a toxin produced by a sea snail, and hope to develop this as a new pain killer.”

Dr Jamieson said innovative new strategies are required for drug discovery that can provide highly potent drugs with no side-effects. Access to these new building blocks is the first step in developing their innovative new protein drug strategy.



Memory Slips in Senior Years and Dementia Risk

(WebMD) Healthy elderly people who begin reporting memory lapses are significantly more likely to be diagnosed with dementia roughly a decade later, new research suggests.

Evaluating more than 500 seniors, scientists found that those with memory complaints were almost three times more likely to develop mild cognitive impairment (memory and thinking problems) — a potential precursor to Alzheimer’s disease — within nine years. Additionally, 80 percent had full-blown dementia within a dozen years.

“I would say if you’re an elderly person and you’re noticing serious changes in your memory, you should take it seriously, but it’s certainly not a cause for immediate alarm,” said study author Richard Kryscio, associate director of University of Kentucky’s Sanders-Brown Center on Aging.

“If you’re a middle-aged person, I would sort of ignore this,” he added. “The average age of the people we started [the study] with was 73… and nothing happened until they were in their 80s, so there’s plenty of time.”

The study is published in the Sept. 24 online edition of the journal Neurology.

Alzheimer’s disease is the most common type of dementia. It causes profound memory loss that is also characterized by impairments in language, focus, judgment and visual perception, according to the Alzheimer’s Association. About 5.2 million Americans have been diagnosed with Alzheimer’s, which is progressive, incurable and eventually leads to death.

The study participants were asked annually about any noticeable changes in their memory, and took memory and thinking tests, for an average of 10 years. After death, 243 participants’ brains were examined for evidence of Alzheimer’s disease during autopsies.

Among other results, nearly 56 percent of participants reported memory lapses overall, at an average age of 82. People carrying a gene increasing the risk of Alzheimer’s had double the odds of experiencing brain impairment. Smokers complaining of memory problems took less time to transition to mild cognitive impairment, the findings showed.

Kryscio said he was mildly surprised to see how many years it took for dementia to set in among those experiencing earlier memory lapses. This extended period potentially offers time to prevent further problems from developing, he noted, but no proven dementia interventions currently exist.

Dr. Anton Porsteinsson, director of the Alzheimer’s Disease Care, Research and Education Program at University of Rochester School of Medicine in New York, called the study “well thought-out.” He said its focus mirrors that of much other research in the field.

Despite the lack of proven dementia interventions, Porsteinsson said, certain lifestyle changes can help memory, including quality sleep, exercise, a healthy diet and brain-stimulating activities.

“Those are things that are reasonable to initiate, especially in those getting worried or noticing some changes in their memory,” he said.

“The challenge here, in terms of interventions, is that there is no single thing that offers a solution,” Porsteinsson added. ”

But for now, for people who do feel their memory is changing in a consistent or significant way, it makes sense for them to at least bring this up with their health care provider and consider whether some changes in lifestyle can contribute to healthy cognitive aging.”