Archives for December 2017

Alzheimer’s Semipostal Fundraising Stamp Dedicated

(NIH) Postmaster General Megan J. Brennan dedicated a stamp today to fund research to help find a cure for one of the top 10 leading causes of death — Alzheimer’s.

Alzheimer's first class stamp; older woman, with someone's hand on her shoulder.

The first-day-of-issue dedication ceremony for the Alzheimer’s Semipostal Fundraising stamp took place at Johns Hopkins Bayview Medical Center in Baltimore. Please share the news on social media using the hashtag #AlzheimersStamp.

The price of the stamp includes the First-Class Mail single-piece postage rate in effect at the time of purchase plus an amount to fund Alzheimer’s research. By law, revenue from sales of the Alzheimer’s Semipostal stamp — minus the postage paid and the reimbursement of reasonable costs incurred by the Postal Service — will be distributed to the National Institutes of Health, which is part of the U.S. Department of Health and Human Services.

“The Postal Service is proud to issue this stamp today to help raise public awareness of Alzheimer’s,” said Brennan.

“Proceeds from its sale will help support urgently needed medical research into this incredibly debilitating disease.”

Joining Brennan in the ceremony were National Institute of Health Deputy Director of the National Institute on Aging Dr. Marie A. Bernard and Johns Hopkins Bayview Medical Center President Dr. Richard Bennett. Johns Hopkins Bayview Medical Center Memory and Alzheimer’s Treatment Center Director Dr. Constantine Lyketsos served as master of ceremonies.

“We’re in a new age of Alzheimer’s research with a number of efforts underway,” said Bernard.

“NIA is working to identify new genes that affect Alzheimer’s disease and their role as risk factors or protective factors, to explore imaging techniques and ways to detect development of the disease well before symptoms appear, to develop and test new therapies, and to test and implement new approaches to providing care and supporting caregivers. The new semipostal stamp will both raise awareness of Alzheimer’s research and care, as well as contribute to the search for effective ways to prevent and treat this heart-breaking disease.”

“Johns Hopkins Bayview has a long history of geriatric care and research,” said Bennett.

“We are honored to host the dedication of the United States Postal Service’s Alzheimer’s Semipostal stamp. Proceeds from the sale of this beautiful stamp will benefit the next generation of research at the National Institutes of Health. We hope this research will lead to new answers for our patients and their families who live with the everyday realities of Alzheimer’s disease.”

Also attending was Kathy Siggins of Mount Airy, MD, who followed the discretionary semipostal program criteria for submitting the stamp suggestion. Siggins’ husband succumbed to the disease in 1999.

The artwork is an illustration that first appeared on the 2008 42-cent Alzheimer’s Awareness stamp. It shows an older woman in profile with a hand on her shoulder, the suggestion of sunlight behind her, and clouds in front of and below her. On the 2008 stamp, she was facing left; the artwork for this stamp shows her facing right to help differentiate between the two stamps. Stamp artist Matt Mahurin of Topanga Canyon, CA, worked under the direction of art director Ethel Kessler of Bethesda, MD.

A Heart-Breaking Disease Affecting Millions of Individuals and Caregivers

According to the Centers for Disease Control, Alzheimer’s is one of the top 10 leading causes of death in the United States. It destroys the minds of those affected by it and poses challenges for family members and caregivers. It is the most common form of dementia, but is not a normal part of aging.

The disease is named after Alois Alzheimer, the German physician who in 1906 discovered and described two hallmark signs of the disease in the brain — clumps of amyloid protein fragments and tangles of tau protein fibers — and linked them to observable symptoms.

Symptoms can include:

  • loss of memory;
  • problems with speech and language;
  • inability to perform familiar daily tasks;
  • trouble interpreting visual images, spatial relationships, and other sensory information; and
  • changes in personality and behavior such as depression, apathy and agitation.

While there is not yet a cure for Alzheimer’s or a way to prevent it, public support has intensified the search for ways to treat its symptoms, slow its progression, and care for those who live with the disease. In 2012, the U.S. Department of Health and Human Services released a “National Plan to Address Alzheimer’s Disease” that addresses the many challenges faced by patients, researchers and caregivers. The plan offered a coordinated effort to prevent and effectively treat the disease by the year 2025 and called for improvements in clinical and long-term care.

According to the Alzheimer’s Association, more than 5.3 million Americans age 65 and older are estimated to have Alzheimer’s disease, a number predicted to rise as the population ages. Net proceeds from this stamp will be distributed to the U.S. Department of Health and Human Services, all part of a national effort to find ways to prevent, treat, and someday stop this disease.

The Semipostal Authorization Act, Pub. L. 106–253, grants the Postal Service discretionary authority to issue and sell semipostal fundraising stamps to advance such causes as it considers to be ”in the national public interest and appropriate.”

Under the program, the Postal Service intends to issue five semipostal fundraising stamps over a 10-year period, with each stamp to be sold for no more than two years. The Alzheimer’s Semipostal stamp is the first and will be followed by a Post-Traumatic Stress Disorder (PTSD) semipostal stamp to be issued in 2019. The next three discretionary semipostal stamps have not yet been determined.


There’s Still No Proven Way to Prevent Alzheimer’s

(HealthDay News) Medical science has failed to prove that any treatment, therapy or brain exercise can help prevent dementias such as Alzheimer’s disease, an extensive new review has concluded.

No medications, over-the-counter remedies or brain training programs have been proven in solid clinical trials to ward off dementia, researchers with the Minnesota Evidence-Based Practice Center in Minneapolis stated after reviewing dozens of previously published studies.

“The upshot is there isn’t a magic bullet,” said review co-author Mary Butler, co-director of the center and an assistant professor with the University of Minnesota School of Public Health.

The best evidence the investigators found indicates that healthy living is a person’s best defense against dementia, Butler said. That means eat right, exercise, treat health problems such as high blood pressure, and remain socially active.

“Of those interventions we were able to find that were tested, the few that showed potential for benefit or even hinting at benefit are really very similar to the kinds of public health messages we put out there in general about healthy aging,” Butler said.

The researchers conducted four side-by-side evidence reviews to test different categories of proposed therapies and treatments for Alzheimer’s:

  • Physical activity. Low-strength evidence from 16 trials showed that combining different types of activity — exercise, diet and cognitive training — might improve performance on brain tests.
  • Prescription drugs. No medications appeared to protect the brain in data from 51 trials. The drugs studied included those specifically for dementia as well as drugs to treat other health problems of aging, such as diabetes, high blood pressure, elevated cholesterol and ebbing hormone levels.
  • Vitamins and supplements. There’s no evidence from 38 trials that any over-the-counter tablets or pills can prevent dementia or Alzheimer’s disease. This included omega-3 fatty acids, ginkgo biloba and vitamins B, C, D and E.
  • Cognitive training. Brain exercises did not ward off dementia in 11 clinical trials.

“There is some moderate evidence that cognitive engagement brings some benefits, but those benefits are local,” Butler said.

“If we train on memory, our memory might improve. If we train on processing, our processing speed might improve. But there isn’t any good evidence to directly link that to changes in how many people develop dementia.”

Dean Hartley, director of science initiatives at the Alzheimer’s Association, said people shouldn’t be discouraged by this review. It doesn’t rule out any possible treatments for dementia — it just notes that science hasn’t proven that any of them work.

“What we need is more research, and that’s what this brings to light,” Hartley said.

Further, it’s a good sign that some evidence indicates that lifestyle changes like exercise and a healthy diet can help with dementia, Hartley continued.

“We can all be doing these now because they aren’t things that are going to hurt us, and will generalize to our health,” he said. “A healthy heart is a healthy brain. We will see that benefit to the brain.”

Alzheimer’s researcher Dr. Luca Giliberto also sees the evidence review as positive, but from a different angle: He hopes the review will shake up the field of research.

“Finally, somebody had the guts to state the fact that we don’t understand what’s going on with dementia and Alzheimer’s,” said Giliberto, an assistant professor with the Feinstein Institute for Medical Research in Manhasset, N.Y. “There’s nothing we currently are able to do to stop Alzheimer’s pathology.”

Researchers need to return to the basics and focus on figuring out why people develop Alzheimer’s before they start testing cures, he said.

“We have to go back to the bench and reinvent the pathology, reinvent everything about Alzheimer’s and these types of dementias,” Giliberto said. “We do not know enough, and we need to stop spending money and time on minor things like supplements and so forth because they are not the answer.”

If nothing else, these studies should lead seniors to stop spending money on online brain training programs, Butler said.

“There just isn’t anything to support that kind of financial expenditure for people with limited financial resources,” she said. “There are probably better things you can do with your time and resources than that. It might just be plain more enjoyable to spend time with people rather than chasing a computer screen.”

People also should be wary of purported “cures” or “preventions” for Alzheimer’s, said Dr. Gisele Wolf-Klein, director of geriatric education with Northwell Health in New Hyde Park, N.Y.

“None of the medications that have been looked at so far have been proven to reverse or even slow down significantly the degradation of cognition,” Wolf-Klein said.

“That doesn’t mean that in the future we won’t be able to find something,” she said. “But as of today, all the prescription medications have failed to slow down or provide cognitive protection.”

The researchers’ findings, presented in four reviews, are published in the Dec. 19 issue of Annals of Internal Medicine.


SOURCES: Mary Butler, Ph.D., co-director, Minnesota Evidence-Based Practice Center and assistant professor, University of Minnesota School of Public Health; Dean Hartley, Ph.D., director of science initiatives, Alzheimer’s Association; Luca Giliberto, M.D., Ph.D., assistant professor, Feinstein Institute for Medical Research, Manhasset, N.Y.; Gisele Wolf-Klein, M.D., director, geriatric education, Northwell Health, New Hyde Park, N.Y.; Dec. 19, 2017, Annals of Internal Medicine

HealthDay Copyright (c) 2017 HealthDay. All rights reserved.


What’s The Connection Between Hearing and Cognitive Health?

(NIH) Hearing loss occurs in approximately one in three people age 65 to 74 and nearly one in two people age 75 and older in the United States, making it one of the most common conditions affecting older adults. Last year, the National Academies of Sciences, Engineering, and Medicine released Hearing Health Care for Adults: Priorities for Improving Access and Affordability, a report that highlights the importance of hearing health to communication and overall quality of life, and proposes recommendations to increase the availability and affordability of hearing health care.

Doctor checking a patient's ears

NIA-funded research has indicated that hearing loss may impact cognition and dementia risk in older adults. A 2011 study found that older adults with hearing loss were more likely to develop dementia than older adults with normal hearing.

In fact, there was a relationship between level of uncorrected hearing loss and level of dementia risk: mild hearing loss was associated with a two-fold increase in risk; moderate hearing loss with a three-fold increase in risk, and severe hearing loss with a five-fold increase in risk. (Lin et al., 2011).

Furthermore, a more recent study found that cognitive abilities (including memory and concentration) declined faster in older adults with hearing loss, as compared to older adults with normal hearing (Lin et al., 2013). These observations by scientists raise the question: can cognitive decline and/or dementia onset be slowed or stopped by correcting hearing loss?

Trial Launched to Test Hearing Intervention Impact on Cognitive Decline

The NIA has recently funded the Aging, Cognition, and Hearing Evaluation in Elders (ACHIEVE) clinical trial led by Drs. Frank Lin and Josef Coresh at Johns Hopkins University to examine the potential benefits of hearing rehabilitation. ACHIEVE will recruit 850 cognitively normal adults aged 70-84 with hearing loss from four locations (Hagerstown MD, Jackson MS, Minneapolis MN, and Winston-Salem NC). Individuals will be randomly assigned to either the hearing intervention (hearing needs assessment, fitting of hearing devices, education/counseling) or control intervention (health education).

ACHIEVE participants will be followed for three years and information on hearing function, cognition, and demographics (e.g. age, sex, education level) will be collected at several timepoints. The primary outcome of the study will be to determine if the hearing rehabilitative intervention changes the rates of cognitive decline as compared to the group receiving health education. Additionally, the researchers will examine if the intervention impacts physical and social functioning, quality of life, and physical activity.

This trial should further our knowledge on the relationship between age-related hearing loss and cognition and dementia. For further information on the trial, please visit .



Lin FR, Metter EJ, O’Brien RJ, Resnick SM, Zonderman AB, Ferrucci L. Hearing loss and incident dementia. Arch Neurol. 2011;68(2):214–220.

Lin FR, Yaffe K, Xia J, Xue Q, Harris TB, Purchase-Helzner E, Satterfield S, Ayonayon HN, Ferrucci L, Simonsick EM, Health ABC Study Group. Hearing loss and cognitive decline in older adults. JAMA Intern Med. 2013;173(4):293–299.


Pharmacologic Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia

2017 Dec 19. doi: 10.7326/M17-1529. [Epub ahead of print]

Pharmacologic Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia: A Systematic Review.

Fink HA1, Jutkowitz E1, McCarten JR1, Hemmy LS1, Butler M1, Davila H1, Ratner E1, Calvert C1, Barclay TR1, Brasure M1, Nelson VA1, Kane RL1.



Optimal treatment to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia is uncertain.


To summarize current evidence on the efficacy and harms of pharmacologic interventions to prevent or delay cognitive decline, MCI, or dementia in adults with normal cognition or MCI.

Data Sources

Several electronic databases from January 2009 to July 2017, bibliographies, and expert recommendations.

Study Selection

English-language trials of at least 6 months’ duration enrolling adults without dementia and comparing pharmacologic interventions with placebo, usual care, or active control on cognitive outcomes.

Data Extraction

Two reviewers independently rated risk of bias and strength of evidence; 1 extracted data, and a second checked accuracy.

Data Synthesis

Fifty-one unique trials were rated as having low to moderate risk of bias (including 3 that studied dementia medications, 16 antihypertensives, 4 diabetes medications, 2 nonsteroidal anti-inflammatory drugs [NSAIDs] or aspirin, 17 hormones, and 7 lipid-lowering agents).

In persons with normal cognition, estrogen and estrogen-progestin increased risk for dementia or a combined outcome of MCI or dementia (1 trial, low strength of evidence); high-dose raloxifene decreased risk for MCI but not for dementia (1 trial, low strength of evidence); and antihypertensives (4 trials), NSAIDs (1 trial), and statins (1 trial) did not alter dementia risk (low to insufficient strength of evidence).

In persons with MCI, cholinesterase inhibitors did not reduce dementia risk (1 trial, low strength of evidence).

In persons with normal cognition and those with MCI, these pharmacologic treatments neither improved nor slowed decline in cognitive test performance (low to insufficient strength of evidence).

Adverse events were inconsistently reported but were increased for estrogen (stroke), estrogen-progestin (stroke, coronary heart disease, invasive breast cancer, and pulmonary embolism), and raloxifene (venous thromboembolism).


High attrition, short follow-up, inconsistent cognitive outcomes, and possible selective reporting and publication.


Evidence does not support use of the studied pharmacologic treatments for cognitive protection in persons with normal cognition or MCI.

Primary Funding Source

Agency for Healthcare Research and Quality.


Copyright © 2017 American College of Physicians. All Rights Reserved.

Physical Activity Interventions in Preventing Cognitive Decline and Alzheimer-Type Dementia

2017 Dec 19. doi: 10.7326/M17-1528. [Epub ahead of print]

Physical Activity Interventions in Preventing Cognitive Decline and Alzheimer-Type Dementia: A Systematic Review.

Brasure M1, Desai P1, Davila H1, Nelson VA1, Calvert C1, Jutkowitz E1, Butler M1, Fink HA1, Ratner E1, Hemmy LS1, McCarten JR1, Barclay TR1, Kane RL1.



The prevalence of cognitive impairment and dementia is expected to increase dramatically as the population ages, creating burdens on families and health care systems.


To assess the effectiveness of physical activity interventions in slowing cognitive decline and delaying the onset of cognitive impairment and dementia in adults without diagnosed cognitive impairments.

Data Sources

Several electronic databases from January 2009 to July 2017 and bibliographies of systematic reviews.

Study Selection

Trials published in English that lasted 6 months or longer, enrolled adults without clinically diagnosed cognitive impairments, and compared cognitive and dementia outcomes between physical activity interventions and inactive controls.

Data Extraction

Extraction by 1 reviewer and confirmed by a second; dual-reviewer assessment of risk of bias; consensus determination of strength of evidence.

Data Synthesis

Of 32 eligible trials, 16 with low to moderate risk of bias compared a physical activity intervention with an inactive control. Most trials had 6-month follow-up; a few had 1- or 2-year follow-up. Evidence was insufficient to draw conclusions about the effectiveness of aerobic training, resistance training, or tai chi for improving cognition. Low-strength evidence showed that multicomponent physical activity interventions had no effect on cognitive function. Low-strength evidence showed that a multidomain intervention comprising physical activity, diet, and cognitive training improved several cognitive outcomes. Evidence regarding effects on dementia prevention was insufficient for all physical activity interventions.


Heterogeneous interventions and cognitive test measures, small and underpowered studies, and inability to assess the clinical significance of cognitive test outcomes.


Evidence that short-term, single-component physical activity interventions promote cognitive function and prevent cognitive decline or dementia in older adults is largely insufficient. A multidomain intervention showed a delay in cognitive decline (low-strength evidence).


Copyright © 2017 American College of Physicians. All Rights Reserved.


Over-the-Counter Supplement Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia

2017 Dec 19. doi: 10.7326/M17-1530. [Epub ahead of print]

Over-the-Counter Supplement Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia: A Systematic Review.

Butler M1, Nelson VA1, Davila H1, Ratner E1, Fink HA1, Hemmy LS1, McCarten JR1, Barclay TR1, Brasure M1, Kane RL1.



Optimal interventions to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia are uncertain.


To summarize the evidence on efficacy and harms of over-the-counter (OTC) supplements to prevent or delay cognitive decline, MCI, or clinical Alzheimer-type dementia in adults with normal cognition or MCI but no dementia diagnosis.

Data Sources

Multiple electronic databases from 2009 to July 2017 and bibliographies of systematic reviews.

Study Selection

English-language trials of at least 6 months’ duration that enrolled adults without dementia and compared cognitive outcomes with an OTC supplement versus placebo or active controls.

Data Extraction

Extraction performed by a single reviewer and confirmed by a second reviewer; dual-reviewer assessment of risk of bias; consensus determination of strength of evidence.

Data Synthesis

Thirty-eight trials with low to medium risk of bias compared ω-3 fatty acids, soy, ginkgo biloba, B vitamins, vitamin D plus calcium, vitamin C or β-carotene, multi-ingredient supplements, or other OTC interventions with placebo or other supplements. Few studies examined effects on clinical Alzheimer-type dementia or MCI, and those that did suggested no benefit. Daily folic acid plus vitamin B12 was associated with improvements in performance on some objectively measured memory tests that were statistically significant but of questionable clinical significance. Moderate-strength evidence showed that vitamin E had no benefit on cognition. Evidence about effects of ω-3 fatty acids, soy, ginkgo biloba, folic acid alone or with other B vitamins, β-carotene, vitamin C, vitamin D plus calcium, and multivitamins or multi-ingredient supplements was either insufficient or low-strength, suggesting that these supplements did not reduce risk for cognitive decline. Adverse events were rarely reported.


Studies had high attrition and short follow-up and used a highly variable set of cognitive outcome measures.


Evidence is insufficient to recommend any OTC supplement for cognitive protection in adults with normal cognition or MCI.

Primary Funding Source

Agency for Healthcare Research and Quality.


Copyright © 2017 American College of Physicians. All Rights Reserved.


Lithium in Water Associated with Slower Rate of Alzheimer’s Disease Deaths

(Journal of Alzheimer’s Disease) Trace elements of lithium in drinking water can slow death rates from Alzheimer’s disease, Brock University research has found.

Rates of diabetes and obesity, which are important risk factors for Alzheimer’s disease, also decrease if there is a particular amount of lithium in the water, says the study, published recently in the Journal of Alzheimer’s Disease.

Postdoctoral fellow Val Fajardo and Rebecca MacPherson, Assistant Professor in the Department of Health Sciences, collected statistics on various lithium levels in drinking water in 234 counties across Texas.

Lithium is a water-soluble alkali metal found in igneous rocks and mineral springs. It is commonly used to treat bipolar and other mood disorders, but at much higher doses than what occurs naturally in drinking water.

The research team, which included Associate Professor of Health Sciences Paul LeBlanc, compared lithium levels naturally found in tap water with Alzheimer’s disease mortality rates, along with the incidence of obesity and diabetes, in the Texas counties.

“We found counties that had above the median level of lithium in tap water (40 micrograms per litre) experienced less increases in Alzheimer’s disease mortality over time, whereas counties below that median level had even higher increases in Alzheimer’s deaths over time,” says Fajardo.

The frequency of obesity and Type 2 diabetes also went down when the drinking water contained similar lithium levels, the researchers found.

Fajardo says he and his team focused on Texas because data on lithium levels were “freely available.”

Previous studies have demonstrated lithium’s ability to protect against Alzheimer’s disease, obesity and diabetes.

“However, we are one of the first groups to show that lithium’s potential protective effect against Alzheimer’s disease, obesity and diabetes may translate to the population setting through very low levels of lithium in tap water,” says Fajardo.

The Brock research comes on the heels of an August study from the University of Copenhagen linking high lithium levels in drinking water to decreases in dementia rates.

But Fajardo warns it’s too early to start advising authorities to add lithium to drinking water.

“There’s so much more research we have to do before policy-makers look at the evidence and say, OK, let’s start supplementing tap water with lithium just like we do in some municipalities with fluoride to prevent tooth decay,” he says.


Journal of Alzheimer’s Disease is published by IOS Press

Copyright © 2017


Inflammation Drives Progression of Alzheimer’s

(DZNE & University of Bonn) According to a study by scientists of the German Center for Neurodegenerative Diseases (DZNE) and the University of Bonn now published in the journal Nature, inflammatory mechanisms caused by the brain’s immune system drive the progression of Alzheimer’s disease. These findings, which rely on a series of laboratory experiments, provide new insights into pathogenetic mechanisms that are believed to hold potential for tackling Alzheimer’s before symptoms manifest. The researchers envision that one day this may lead to new ways of treatment. Further institutions both from Europe and the US also contributed to the current results.

Alzheimer’s disease is a devastating neurodegenerative condition ultimately leading to dementia. An effective treatment does not yet exist. The disease is associated with the aberrant aggregation of small proteins called “Amyloid-beta” (Abeta) that accumulate in the brain and appear to harm neurons.

In recent years, studies revealed that deposits of Abeta, known as “plaques,” trigger inflammatory mechanisms by the brain’s innate immune system. However, the precise processes that lead to neurodegeneration and progression of pathology have thus far not been fully understood.

“Deposition and spreading of Abeta pathology likely precede the appearance of clinical symptoms such as memory problems by decades. Therefore, a better understanding of these processes might be a key for novel therapeutic approaches. Such treatments would target Alzheimer’s at an early stage, before cognitive deficits manifest,” says Prof. Michael Heneka, a senior researcher at the DZNE and Director of the Department of Neurodegenerative Diseases and Gerontopsychiatry at the University of Bonn.

An Inflammatory Cascade

Prof. Heneka, who is also involved in the cluster of excellence “ImmunoSensation” at the University of Bonn, and coworkers have been investigating the role of the brain’s immune response in the progression of Abeta pathology for some time already.

Previous work by the group that was published in Nature in 2013, had established that the molecular complex NLRP3, which is an innate immune sensor, is activated in brains of Alzheimer’s patients and contributes to the pathogenesis of Alzheimer’s in the murine model. NLRP3 is a so-called inflammasome that triggers production of highly pro-inflammatory cytokines.

Furthermore, upon activation, NLRP3 forms large signaling complexes with the adapter protein ASC, which are called “ASC specks” that can be released from cells.

“The release of ASC specks from activated cells has so far only been documented in macrophages and their relevance in disease processes has so far remained a mystery,” says Prof. Eicke Latz, director of the Institute of Innate Immunity and member of the cluster of excellence “ImmunoSensation” at the University of Bonn.”

Inflammatory proteins (called “ASC specks”, red) within the nucleus of an aggregate of Amyloid-beta peptides (blue). Furthermore, immune cells (green) are shown. Researchers of the DZNE and the University of Bonn report in “Nature” on the role of inflammatory mechanisms in Alzheimer’s disease. Image reconstruction of microscopy imaging data by Dario Tejera, University of Bonn.

Connection between Inflammation and Neurodegeneration

In the current study, it was demonstrated that ASC specks are also released from activated immune cells in the brain, the “microglia.” Moreover, the findings provide a direct molecular link to classical hallmarks of neurodegeneration.

“We found that ASC specks bind to Abeta in the extracellular space and promote aggregation of Abeta, thus directly linking innate immune activation with the progression of pathology,” Heneka says.

Novel Approach for Therapy?

This view is supported by a series of experiments in mouse models of Alzheimer’s disease. In these, the researchers investigated the effects of ASC specks and its component, the ACS protein, on the spreading of Abeta deposits in the brain.

“Additionally, analysis of human brain material indicates at several levels that inflammation and Abeta pathology may interact in a similar fashion in humans. Together our findings suggest that brain inflammation is not just a bystander phenomenon, but a strong contributor to disease progression,” Heneka says.

“Therefore, targeting this immune response will be a novel treatment modality for Alzheimer’s.”



Journal Reference:

Carmen Venegas, Sathish Kumar, Bernardo S. Franklin, Tobias Dierkes, Rebecca Brinkschulte, Dario Tejera, Ana Vieira-Saecker, Stephanie Schwartz, Francesco Santarelli, Markus P. Kummer, Angelika Griep, Ellen Gelpi, Michael Beilharz, Dietmar Riedel, Douglas T. Golenbock, Matthias Geyer, Jochen Walter, Eicke Latz, Michael T. Heneka. Microglia-derived ASC specks cross-seed amyloid-β in Alzheimer’s diseaseNature, 2017; 552 (7685): 355 DOI: 10.1038/nature25158