Archives for December 2016

Apps to Help Caregivers Stay Organized

(AARP) Try these free tools for scheduling, record keeping, sharing and more.

There is so much technology now targeted toward caregivers; how do you find the tools that will be the most helpful? In a previous column I shared some basic tips to keep in mind when choosing caregiving technology. Now I’m focusing on three specific apps that can help caregivers get (and stay) organized.

The apps outlined below fit my criteria: They’re user-friendly and available in iOS (iPhone/iPad), on Android and on a website. They synchronize across devices — meaning you can make a change on your phone or tablet and it will automatically appear on your computer, or vice versa. They’re also secure and password protected (be sure you choose a strong password since you will be entering personal information). They also happen to be free.


CareZone is the most comprehensive app for managing overall caregiving duties, including coordination of friends and family, health care record keeping and scheduling with a shareable calendar.

Some key features:

  • Medications — Create a medication list by simply taking photos of the medication labels; set up medication reminders.
  • Services — Access CareZone Pharmacy services with free pill packaging and auto-refills; print anything in your CareZone; send medication lists.
  • Trackers — Log and track health information such as weight, mood, sleep, pain, blood pressure and blood glucose.
  • Journal — Record significant events, health issues, doctor appointments and more.
  • Contacts — Import contacts for doctors, care providers and team members from your phone contacts, or create new contacts in the app or online. Share them with team members.
  • Photos and files — Add photos and document files such as doctor lists, copies of insurance cards or advanced directives.
  • Sharing — Invite others to share access to facilitate team coordination or in an emergency.

Pros: This app, also available for Apple Watch, combines many useful functions in one handy place. The ability to upload key document files online (such as a power of attorney) and access them on a phone or tablet — as well as send them to someone from there — is convenient. For customer service, you can send an email message with questions, and in the online version there is a “knowledge base” (FAQ).

Cons: The Journal and Notes sections don’t include the ability to search by keywords or tags. The “To Do List” feature cannot be organized by categories, and you can’t easily assign or have someone volunteer to do tasks.


The CaringBridge app allows you to create a site for yourself or the person you’re caring for and invite family and friends to join. It’s intended for a larger group of family and friends to stay updated, coordinate caregiving help and post notes of support.

Some key features:

  • Privacy — Choose whether visitors must sign up and log in, and whether you only want to allow people you invite to join.
  • Journal — Post updates and photos (which are also then available in the Photos section of the app).
  • Planner/calendar — Share key dates and create appointments and tasks for which people can volunteer to assist (including a feature to easily add the appointment address that users can view on a map). You can also click “Add to calendar” to add the appointment to your personal phone or computer default calendar.
  • Fundraising — Help start a personal fundraising effort (presumably to pay for health care) via CaringBridge’s partnership with GoFundMe.

Pros: The site and app are easy to use and visually appealing. It’s one of few apps that include a phone number for customer support, but you can also email questions to the customer care team, and there is a long list of “published answers” (FAQs).

Cons: New features available on the website (personal fundraising and site links) aren’t available on the phone app, and FAQs are difficult to find in the phone/tablet app version. The appeal for donations is a bit too frequent for my taste.

Lotsa Helping Hands

LotsaHelpingHands is best for creating a connected community with family and friends where you can post news, and for coordinating assistance for your loved one through a shared calendar.

Key features:

  • Help Calendar — Schedule activities so people can volunteer for specific things, such as meal prep or rides to appointments. Volunteers receive reminders before their activities.
  • Announcements — Post updates with notes and photos.
  • Well Wishes — Users can express love and support.

Pros: The app is simple and streamlined, and it’s easy to move between communities if you join more than one. You can easily view the latest posts on the home screen. The online version is complete and easy to navigate.

Cons: The phone app is missing several features available in the online version, including the ability to create activities (they can be created online and will sync to the calendar in the app, but you cannot create activities on your phone).

Tip: Try an app, and if it doesn’t make sense fairly quickly (my personal cutoff time is 10 or 15 minutes), go on to the next one. You don’t have to be able to master every feature in that time, but you should be able to get the gist of it and find all of the components. App use is all about individual preference: What works intuitively for one person may not work as well for another.

Please let me know if there are other apps you’ve found helpful. And stay tuned for my columns on more useful apps and gadgets for caregivers.

Amy Goyer is AARP’s family and caregiving expert and author of AARP’s Juggling Life, Work and Caregiving.

She spends most of her time in Phoenix, where she is caring for her 92-year-old dad, Robert, who has advanced Alzheimer’s disease. Follow her blog and videos and connect with Amy on TwitterFacebook and LinkedIn. For ongoing caregiving support from Amy and AARP, text “AMY” to 97779.


Copyright 2016 AARP


Science Behind the Headlines: Alzheimer’s and Coconut Oil

(Alzheimer’s Society, UK) There have been some claims that coconut oil could be used as a treatment, or even a cure, for Alzheimer’s disease. However, there is currently not enough experimental evidence to back up these claims.

The claim is based on the theory that the neurones (nerve cells) in the brains of people with Alzheimer’s disease are unable to use glucose to produce energy properly and therefore ‘starve’. The theory is that coconut oil may act as an alternative energy source, but there is not enough scientific evidence to know for sure whether this is the case.

There is a clinical trial being conducted in the US, which should provide some evidence as to whether coconut oil is safe to use in people with Alzheimer’s disease and if it has any effects on thinking or memory for people with the condition. The results of this clinical trial are due to be announced in mid-2017.

Why do people think that coconut oil could help in Alzheimer’s disease? 

Insulin, the hormone responsible for regulating blood sugar and glucose, has been linked to changes in the brain associated with Alzheimer’s disease. However, it is not clear exactly what role insulin has in the disease and the hormone has many different roles in the body alongside regulating glucose. This means that the changes associated with dementia could be unconnected to glucose metabolism. Brain cells do appear to have problems with their metabolism in Alzheimer’s disease, but it is unclear whether this is a cause of the disease or is the result of other disease-related processes.

The idea that coconut oil could provide an alternative energy source for brain cells comes from the successful treatment of children with epilepsy with a ketogenic diet. In this diet, carbohydrates are strictly limited and replaced by high fat intakes, forcing the body to use fat as a primary energy source (a similar idea lies behind the Atkins diet). Coconut oil is used to allow a slightly higher level of carbohydrate intake, making the very strict diet slightly easier to follow, but still preventing the body using sugar from carbohydrates as the main energy source. This works only because the body is forced to metabolise fats.

The ketogenic diet must be incredibly strict because the body will always preferentially use glucose for metabolism. Therefore, simply adding coconut oil to the diet would not provide the neurones in the brain with an alternative energy source. The diet is also linked to very high cholesterol levels, which increases risk factors for stroke, heart disease and dementia.

There is also evidence to suggest that fats like coconut oil could indirectly result in increased levels of a protein called acetylcholinesterase. Current treatments for Alzheimer’s disease are ‘acetylcholinesterase inhibitors‘ and work by reducing the levels of this protein. An increase is associated with Alzheimer’s disease, meaning that coconut oil could be detrimental to people with Alzheimer’s disease. This is why it is important to ensure that any potential treatment is safe to use for people with Alzheimer’s disease before it can be approved for widespread use.

Watch our video about coconut oil and dementia (duration 2:05). Read the video transcripts for this film.



All content © 2016 Alzheimer’s Society. Registered office at Devon House, 58 St Katharine’s Way, London E1W 1LB

Alzheimer’s Society is a registered Charity No. 296645. Registered as a company limited by guarantee and registered in England No. 2115499


Federal Update: Alzheimer’s Progress in the 114th Congress

(Alzheimer’s Association) As the 114th session of Congress draws to a close we are excited to share with you some of the incredible progress we’ve achieved in our ongoing efforts to make Alzheimer’s a national priority.

In its final week, Congress passed the 21st Century Cures Act, legislation that will accelerate the discovery, development and delivery of new treatments and cures for many diseases. It also increases funding at the National Institutes of Health for innovative approaches to addressing complex diseases. And it streamlines the regulatory process to ensure that treatments can be available to patients as soon as possible. The 21st Century Cures Act also includes the Ensuring Useful Research Expenditures is Key for Alzheimer’s (EUREKA) Act which will help to advance research breakthroughs for Alzheimer’s disease, and encourage public-private partnerships. Alzheimer’s Association and our strategic partner the Alzheimer’s Impact Movement (AIM) have supported both of these key pieces of legislation since their introduction and we’re excited to announce that last week they were signed into law by the President!

These important actions are just the latest in a series of recent public policy victories for our cause. Indeed, as we look back on the session, one thing is clear — this Congress brought remarkable advancements for our cause because of your relentless efforts.

Since the 114th Congress convened in January 2015, we have progressed on our goal to increase Alzheimer’s research funding at the National Institutes of Health (NIH) — first, with the historic funding annual increase of $350 million for fiscal year 2016, the largest in history, signed into law in December 2015. And again, this summer when the House Appropriations Committee approved an additional $350 million increase for FY17 and the Senate Appropriations Committee approved $400 million. We are encouraged by the growing support for our cause and the return of our champions in Congress. Together with the work of you, our advocates, we will continue the pursuit of this additional FY17 funding when the new Administration and Congress begin their work in January.

The 114th Congress also saw the advancement of critical legislation to increase access to care planning and support services. The Alzheimer’s Association, AIM, and advocates like you led the way on the HOPE for Alzheimer’s Act to provide Medicare coverage for comprehensive care planning services for those living with Alzheimer’s disease and other cognitive impairments. Because of our efforts, congressional cosponsorship numbers soared, and in November 2016, the Centers for Medicare and Medicaid Services (CMS) finalized a decision to pay for cognitive and functional assessments and care planning. In 2017, for the first time, people living with Alzheimer’s will have access to care planning with a medical professional covered by Medicare. also saw support grow for the Palliative Care and Hospice Education and Training Act (PCHETA). PCHETA would ensure an adequate, well-trained palliative care workforce through workforce training, education and awareness and enhanced research. Thanks to the leadership and advocacy of the Association, during the 114th Congress PCHETA reached 234 bipartisan cosponsors in the House, and 20 cosponsors in the Senate. We will continue to work to ensure advance this legislation in the new year.

Additionally, there was increased support in Congress for Kevin and Avonte’s Law, which reauthorizes the Missing Alzheimer’s Disease Patient Alert Program to help reduce injury and death of Americans with Alzheimer’s and developmental disabilities. This program is a proven success, helping law enforcement quickly identify and reunite persons with Alzheimer’s with their families and caregivers. Our advocates have again been relentless in efforts to build support for this legislation, growing the number of co-sponsors in the House from 23 in late August to 93 today. While, the 114th Congress departed before taking final action on the legislation, the support we have helped garner for the bill has us hopeful for its passage in the new Congress.

For all these tremendous developments there is much more work to be done. As we look ahead to the incoming Administration and the 115th Congress, we are already hard at work with the new and returning leadership to advance public policy solutions that will improve the lives of those living with Alzheimer’s disease and their caregivers. To learn about these efforts and how you can get involved visit We also invite you to join us for the 2017 Alzheimer’s Association Advocacy Forum in Washington D.C.

None of this would be possible without you. Thank you for all of your contributions to making these advances possible and to bringing us another step closer to realizing our vision of a world without Alzheimer’s.


© 2016 Alzheimer’s Association. All rights reserved.


Elder Care for Alzheimer’s: Choosing a Provider

(MayoClinic) Elder care (adult care) can provide an opportunity for your loved one with Alzheimer’s to receive assistance and therapeutic activities in a group setting.

Being a full-time caregiver can be tiring and time-consuming. Elder care can provide you with a temporary break to relax, to get errands done or to complete housework. Also, elder care may be an option for your loved one if you work full time during the day.

In the U.S. you can locate elder care services available in your area by using the Department of Health and Human Services’ Eldercare Locator website. This website provides contact information for your state or local area agency on aging (AAA). The AAA will connect you with someone who will help guide you to specific elder care service providers.

Determine Your Needs

When considering elder care providers, evaluate the services your loved one may need, including:

  • Socialization
  • Supervision
  • Behavior management, such as needing to be watched so that he or she doesn’t wander off
  • Counseling
  • Activities, such as art, music, recreation or support groups
  • Exercise
  • Physical, occupational or speech therapy
  • Medical care
  • Medication management
  • Meals and nutrition
  • Personal care, such as bathing and eating
  • Special needs, such as needing wheelchair access

If you’re choosing among more than one provider, some additional considerations are:

  • Location. How convenient is it?
  • Hours. What are drop-off and pickup times? Does your loved one need to attend a minimum number of hours or days a week? Does the provider need notice if your loved one will not be attending one day?
  • Costs. Often, costs are out-of-pocket, but some long-term care insurance plans may cover this type of care. Some providers offer options, such as allowing you to pay a certain amount depending on your income. Ask your provider about all fees involved in elder care. Costs may vary depending on the services available and the provider’s location.
  • Services and programs. What services and programs are offered?
  • Group activities. Are people with Alzheimer’s in a separate group from other people or are they included in group activities?
  • Your loved one’s needs. How does the provider determine your loved one’s needs?
  • Staff. Is the staff trained in working with people with Alzheimer’s disease? What health care professionals are on staff? How does the provider screen staff? What are the provider’s staffing ratios?
  • Safety. How does this provider ensure the safety of every person?
  • Emergencies. How does this provider deal with emergency situations?
  • Transportation. Does the provider have transportation available for people who may need it?

Ensuring Quality Care

Entrusting your loved one to someone else’s care can be difficult. When you’re choosing a center, here are some suggestions to consider to ensure that your loved one will get quality care:

  • Ask for references. Ask other caregivers about their experiences. Ask your physician for recommendations of providers that other patients have endorsed. Ask for references and talk to a few people who have used the provider.
  • Do some research. Ask the AAA representative or a local senior center whether they have any specific information on the facility you’re considering.
  • Ask questions. On a first visit to a potential facility, walk through and ask several questions, including questions about available services, the center’s certification and licenses, and staff training. The National Adult Day Services Association has a site-visit question checklist you can print and take with you.
  • Try it out. When you think you have decided on a center, try it out. Be aware that it may take some time for your loved one to feel comfortable in the new surroundings.

Jonathan Graff-Radford, M.D.

© 1998-2016 Mayo Foundation for Medical Education and Research. All rights reserved.


Feeling Lonely: Alzheimer’s Pathology Gives People Sense of Disconnection

(AlzForum) For some with impending Alzheimer’s, a crowded room begins to feel just as lonely as an empty one. Could this perceived social isolation be an early warning sign of plaque build-up in the brain? According to a paper in the December JAMA Psychiatry, perhaps so.

Scientists led by Reisa Sperling, Brigham and Women’s Hospital, Boston, report that cognitively normal people with amyloid in their brains are 7.5 times more likely to report feeling lonely. The finding points to socioemotional changes, in addition to cognitive and behavioral ones, that could be associated with Alzheimer’s. If the results are replicated in larger cohorts, screening for loneliness could help identify candidates for amyloid scans, scientists said.

“From a statistical perspective, the findings are quite robust,” said José Luis Molinuevo of Barcelonaβeta Brain Research Center in Spain.

“It may be that this is part of the very early symptomatology of the disease that we are not capturing yet.”

Loneliness is a subjective feeling of social and emotional detachment that remains distinct from objective social isolation. In other words, some people may feel alone even when surrounded by people. For instance, geriatric clinician Carla Perissinotto, University of California, San Francisco, recalls a woman who kept weekly social engagements, employed a full-time caregiver, and saw her son every day, but complained that she felt immensely lonely. Conversely, one man who lived alone and saw almost no family during the week said he felt fine.

“I’ve seen it go both ways,” wrote Perissinotto to Alzforum.

“We can’t make assumptions about who is or isn’t lonely.”

Previous studies have associated feeling lonely with memory problems, functional decline, and progression to AD (Donovan et al., 2016; Perissinotto et al., 2012; Wilson et al., 2007). Given the links to impairment and disease, Sperling and colleagues wondered whether loneliness could be related to one of the principal pathologies of Alzheimer’s disease—the accumulation of amyloid plaques.

First author Nancy Donovan and colleagues assessed 79 cognitively and psychiatrically healthy people aged 60 to 90 from the Harvard Aging Brain Study (HABS). In addition to undergoing a positron emission tomography scan with Pittsburgh Compound B (PiB-PET) to measure brain amyloid, each person took a three-question survey to assess how lonely he or she felt. It asked how often people felt left out, isolated from others, or lacking in companionship. They scored 1, 2, 3, or 4 points for answering never, rarely, sometimes, or often, respectively. A person was considered lonely if they answered any of the three questions “sometimes” or “often.”

The researchers also derived a separate social network score, which objectively measured social activity. It accounted for whether a person lived with another, had at least three monthly visitors, and participated in community groups or religious activities. Separate scales assessed anxiety and depression. The researchers also noted whether participants carried the ApoE4 allele.

In this cohort, the average loneliness score was 5.3. The more amyloid a person had in his or her brain, the more likely they were to report feeling lonely. This was even after adjusting for age, sex, ApoE4 status, depression, anxiety, and social network score. When PiB-PET was analyzed as a continuous variable, every 0.1 DVR increase was accompanied by a 75 percent higher chance of feeling lonely.

When the researchers divided the group into amyloid-positive and –negative subjects, almost half of the 25 amyloid-positive folks, but only a third of the 40 amyloid-negative participants, reported being socially withdrawn. That gave those with brain amyloid a 7.5 times higher chance of feeling lonely compared to the negative group. The association was strongest for the 22 people who carried the ApoE4 allele. Interestingly, PiB-PET did not correlate with the objective social network score, suggesting a person with amyloid in the brain could be socially active and yet still feel disconnected.

“It’s a strong effect in this sample,” wrote Michael Weiner, University of California, San Francisco, to Alzforum.

However, the finding needs to be replicated before it becomes established, said Weiner, who was not involved in the study. He added that researchers currently do not assess feelings of social isolation in the Alzheimer’s Disease Neuroimaging Initiative (ADNI), which he leads.

Scientists from other large cohort studies that include amyloid scans, such as the Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL), also confirmed that they do not collect data on loneliness. There are some international cohorts and large epidemiological studies that have incorporated this loneliness assessment to see how the score changes with age, such as the Ann Arbor, Michigan-based Health and Retirement Study (HRS), said Donovan. These studies, however, do not scan for amyloid.

Donovan proposed that while the field understands very little about the neural basis of loneliness, the link with amyloid could result from functional alterations in the default mode network, which takes an early hit in Alzheimer’s disease. The group is in the process of measuring loneliness in the remaining HABS participants, and will follow scores longitudinally to see which changes first.

They also plan to examine whether loneliness correlates with changes in network connectivity or tau buildup using functional magnetic resonance imaging and tau PET. Scientists contacted for this article were unaware of other studies that assess loneliness along with functional brain measures.

If this finding holds up in prospective studies and in other cohorts, loneliness could be added to the algorithms that predict who is most likely to have a positive amyloid PET scan, Molinuevo said. Very few predictive factors are now available—ApoE status, cognitive decline, age—and researchers are actively seeking new ones, he said. Further refining those algorithms would reduce the cost of building trial-ready cohorts, such as the Global Alzheimer’s Platform (GAP) or the European Prevention of Alzheimer’s Dementia (EPAD), which Molinuevo co-leads (Aug 2016 conference news).

Other researchers wrote that loneliness could be the first of many socioemotional factors that characterize the early stages of Alzheimer’s. “Why stop with loneliness?” wrote Paul Rosenberg, Johns Hopkins School of Medicine, Baltimore, in an accompanying commentary.

There may be other emotions yet to be discovered—such as fear, existential angst, dread, or even positive feelings—that could reflect amyloid burden or the presence of other AD biomarkers. Assessing various emotions in older adults while measuring relevant biomarkers could yield clues for further study, he wrote.


By Gwyneth Dickey Zakaib

Copyright © 1996–2016 Biomedical Research Forum, LLC. All Rights Reserved.


New Biomarker Predicts Alzheimer’s Disease and Link to Diabetes

 (Iowa State University) An enzyme found in the fluid around the brain and spine is giving researchers a snapshot of what happens inside the minds of Alzheimer’s patients and how that relates to cognitive decline.

Iowa State University researchers say higher levels of the enzyme, autotaxin, significantly predict memory impairment and Type 2 diabetes. Just a one-point difference in autotaxin levels – for example, going from a level of two to a three – is equal to a 3.5 to 5 times increase in the odds of being diagnosed with some form of memory loss, said Auriel Willette, an assistant professor of food science and human nutrition at Iowa State.

Autotaxin, often studied in cancer research, is an even stronger indicator of Type 2 diabetes. A single point increase reflects a 300 percent greater likelihood of having the disease or pre-diabetes. The results are published in the Journal of Alzheimer’s Disease. Willette and Kelsey McLimans, a graduate research assistant, say the discovery is important because of autotaxin’s proximity to the brain.

“We’ve been looking for metabolic biomarkers which are closer to the brain. We’re also looking for markers that reliably scale up with the disease and have consistently higher levels across the Alzheimer’s spectrum,” Willette said.

“This is as directly inside of the brain as we can get without taking a tissue biopsy.”

Willette’s previous research found a strong association between insulin resistance and memory decline and detrimental brain outcomes, increasing the risk for Alzheimer’s disease. Insulin resistance is a good indicator, but Willette says it has limitations because what happens in the body does not consistently translate to what happens in the brain. That is why the correlation with this new enzyme found in the cerebrospinal fluid is so important.

“It has a higher predictive rate for having Alzheimer’s disease,” McLimans said.

“We also found correlations with worse memory function, brain volume loss and the brain using less blood sugar, which have also been shown with insulin resistance, but autotaxin has a higher predictive value.”

Physical Health Linked to Memory

The fact that autotaxin is a strong predictor of Type 2 diabetes and memory decline emphasizes the importance of good physical health. Researchers say people with higher levels of autotaxin are more likely to be obese, which often causes an increase in insulin resistance.

Willette says autotaxin levels can determine the amount of energy the brain is using in areas affected by Alzheimer’s disease. People with higher autotaxin levels had fewer and smaller brain cells in the frontal and temporal lobes, areas of the brain associated with memory and executive function. As a result, they had lower scores for memory and tests related to reasoning and multitasking.

“Autotaxin is related to less real estate in the brain, and smaller brain regions in Alzheimer’s disease mean they are less able to carry out their functions,” Willette said.

“It’s the same thing with blood sugar. If the brain is using less blood sugar, neurons have less fuel and start making mistakes and in general do not process information as quickly.”

Researchers analyzed data from 287 adults collected through the Alzheimer’s Disease Neuroimaging Initiative, a public-private partnership working to determine whether MRI and PET scans as well as biological markers can measure the progression of cognitive impairment and Alzheimer’s disease. The data came from adults ranging in age from 56 to 89 years old. Study participants completed various tests to measure cognitive function. This included repeating a list of words over various time increments.

The research was supported by an Iowa State Presidential Initiative for Interdisciplinary Research grant and a National Institutes of Health grant.


Journal Reference:

Kelsey E. McLimans, Auriel A. Willette. Autotaxin is Related to Metabolic Dysfunction and Predicts Alzheimer’s Disease Outcomes. Journal of Alzheimer’s Disease, December 2016

Copyright © 1995-2016, Iowa State University of Science and Technology. All rights reserved.


Single Protein May Hold Secret to Treating Parkinson’s Disease and More

(Gladstone Institutes) A new way to regulate protein levels and functions could be the answer to treating devastating neurological conditions.

New details learned about a key cellular protein could lead to treatments for neurodegenerative diseases, such as Parkinson’s, Huntington’s, Alzheimer’s, and amyotrophic lateral sclerosis (ALS).

At their root, these disorders are triggered by misbehaving proteins in the brain. The proteins misfold and accumulate in neurons, inflicting damage and eventually killing the cells. In a new study, researchers in the laboratory of Steven Finkbeiner, MD, PhD, at the Gladstone Institutes used a different protein, Nrf2, to restore levels of the disease-causing proteins to a normal, healthy range, thereby preventing cell death.

The researchers tested Nrf2 in two models of Parkinson’s disease: cells with mutations in the proteins LRRK2 and α-synuclein. By activating Nrf2, the researchers turned on several “house-cleaning” mechanisms in the cell to remove excess LRRK2 and α-synuclein.

“Nrf2 coordinates a whole program of gene expression, but we didn’t know how important it was for regulating protein levels until now,” explained first author Gaia Skibinski, PhD, a staff research scientist at Gladstone.

“Overexpressing Nrf2 in cellular models of Parkinson’s disease resulted in a huge effect. In fact, it protects cells against the disease better than anything else we’ve found.”

In the study, published in the Proceedings of the National Academy of Sciences, the scientists used both rat neurons and human neurons created from induced pluripotent stem cells. They then programmed the neurons to express Nrf2 and either mutant LRRK2 or α-synuclein. Using a one-of-a-kind robotic microscope developed by the Finkbeiner laboratory, the researchers tagged and tracked individual neurons over time to monitor their protein levels and overall health. They took thousands of images of the cells over the course of a week, measuring the development and demise of each one.

The scientists discovered that Nrf2 worked in different ways to help remove either mutant LRRK2 or α-synuclein from the cells. For mutant LRRK2, Nrf2 drove the protein to gather into incidental clumps that can remain in the cell without damaging it. For α-synuclein, Nrf2 accelerated the breakdown and clearance of the protein, reducing its levels in the cell.

“I am very enthusiastic about this strategy for treating neurodegenerative diseases,” said Finkbeiner, a senior investigator at Gladstone and senior author on the paper.

“We’ve tested Nrf2 in models of Huntington’s disease, Parkinson’s disease, and ALS, and it is the most protective thing we’ve ever found. Based on the magnitude and the breadth of the effect, we really want to understand Nrf2 and its role in protein regulation better.”

The scientists say that Nrf2 itself may be difficult to target with a drug because it is involved in so many cellular processes, so they are now focusing on some of its downstream effects. They hope to identify other players in the protein regulation pathway that interact with Nrf2 to improve cell health and that may be easier to drug.

Funding was provided by the National Institutes of Mental Health, National Institute of Neurological Disorders and Stroke, National Human Genome Research Institute, California Institute of Regenerative Medicine, Taube/Koret Center, Michael J. Fox Foundation, ALS Association, National Center for Research Resources, and the Betty Brown family. The work is dedicated to the memory of Nita Hirsch.


Copyright © 2016 by the American Association for the Advancement of Science (AAAS)


“Sniff Test” May Be Useful in Diagnosing Early Alzheimer’s Disease

(Journal of Alzheimer’s Disease) Tests that measure the sense of smell may soon become common in neurologists’ offices. Scientists have been finding increasing evidence that the sense of smell declines sharply in the early stages of Alzheimer’s, and now a new study from the Perelman School of Medicine at the University of Pennsylvania published today in the Journal of Alzheimer’s Disease confirms that administering a simple “sniff test” can enhance the accuracy of diagnosing this dreaded disease.

The sniff test also appears to be useful for diagnosing a pre-dementia condition called mild cognitive impairment (MCI), which often progresses to Alzheimer’s dementia within a few years.

Neurologists have been eager to find new ways to identify people who are at high risk of Alzheimer’s dementia but do not yet show any symptoms. There is a widespread consensus that Alzheimer’s medications now under development may not work after dementia has set in.

“There’s the exciting possibility here that a decline in the sense of smell can be used to identify people at risk years before they develop dementia,” said principal investigator David R. Roalf, PhD, an assistant professor in the department of Psychiatry at Penn.

Roalf and his colleagues used a simple, commercially available test known as the Sniffin’ Sticks Odor Identification Test, in which subjects must try to identify 16 different odors. They administered the sniff test, and a standard cognitive test (the Montreal Cognitive Assessment), to 728 elderly people.

The subjects had already been evaluated by doctors at Penn with an array of neurological methods, and according to expert consensus had been placed in one of three categories: “healthy older adult,” “mild cognitive impairment,” or “Alzheimer’s dementia.” Roalf and his team used the results from the cognitive test alone, or combined with the sniff test, to see how well they identified subjects in each category.

As researchers report, the sniff test added significantly to diagnostic accuracy when combined with the cognitive test.

For example, the cognitive test alone correctly classified only 75 percent of people with MCI, but that figure rose to 87 percent when the sniff test results were added. Combining the two tests also enabled more accurate identification of healthy older adults and those with Alzheimer’s dementia. The combination even boosted accuracy in assigning people to milder or more advanced categories of MCI.

“These results suggest that a simple odor identification test can be a useful supplementary tool for clinically categorizing MCI and Alzheimer’s, and even for identifying people who are at the highest risk of worsening,” Roalf said.

Prompted by prior studies that have linked a weakening sense of smell to Alzheimer’s, doctors in a few larger dementia clinics already have begun to use smell tests in their assessments of elderly patients. Part of the reason the practice has not yet become common is that the tests that seem most useful take too long to administer. Roalf and colleagues are now trying to develop a briefer test that works as well as the longer ones.

“We’re hoping to shorten the Sniffin’ Sticks test, which normally takes 5 to 8 minutes, down to 3 minutes or so, and validate that shorter test’s usefulness in diagnosing MCI and dementia—we think that will encourage more neurology clinics to do this type of screening,” Roalf said.

Roalf and his laboratory also plan to investigate whether protein markers of Alzheimer’s, which are present in the olfactory region of the brain before dementia occurs, can be detected in nasal fluid to provide an even earlier warning of the disease process.

Studies suggest that a high proportion of older adults who have cognitive impairment are not identified as such, in part due to lack of adequate screening.

The study’s first author was Penn’s Megan Quarmley; the other co-authors were Paul J. Moberg, Dawn Mechanic-Hamilton, Sushila Kabadi, and David A. Wolk, all of Penn, and Steven E. Arnold of Harvard University and Massachusetts General Hospital.

Funding was provided by the National Institute of Mental Health (K01 497 MH102609), National Institute on Aging (P30 AG10124), and the Penn Center of Excellence for Research on Neurodegenerative Diseases.



Quarmley M, Moberg PJ, Mechanic-Hamilton D, Kabadi S, Arnold SE, Wolk DA, Roalf DR. Odor Identification Screening Improves Diagnostic Classification in Incipient Alzheimer’s Disease. J Alzheimers Dis. 2016 Nov 18.

Journal of Alzheimer’s Disease is published by IOS Press

Copyright © 2016