Issue 70, January 2016
bullet"Digital Dementia"
bulletResearch Indicates Low Doses of Sleep-Inducing Drugs as Possible Therapy for Alzheimer's
bulletInnovation: Semper - A Micro-learning Memory App
bulletInterview with Internationally Renowned Aging Researcher Prof. Dr. Konrad Beyreuther
bulletVirtual Reality Test Offers New Insight on Alzheimer's Risk Factors
Memory is central to human existence and to the human experience. It governs our ability to learn, tell stories, remember names, recognize faces, and make sense of reality. Memories are also integral to our sense of self. Our life stories - composed of what we've done and with whom we've connected - shape our identities. Moreover, our thoughts about the past influence how we think about the future. Our memories thus lie at the very core of who we are as human beings.

Memory loss, age-related or otherwise, can therefore symbolize a devastating loss of self. In fact, deteriorating cognitive abilities rank among the greatest fears that people have as they age. For these reasons, researchers are actively working on discovering new ways to fend off mental decline as we get older.

Cutting-edge research coming out of Germany is tackling this subject from a variety of angles. This ranges from new research findings indicating that low doses of sleep-inducing drugs may serve as a possible therapy for Alzheimer's to innovative mobile apps that promote effortless learning and retention of new material in today's day and age of information overload.

By attaining a better understanding of our diverse neural architectures, researchers may one day understand why some people are more susceptible to memory loss caused by neurodegenerative diseases and know what can be done to counteract the detrimental effects of such disorders.  

Is technology making us dumb? Is "digital dementia" on the rise? Drawing from studies in cognitive neuroscience, experimental psychology, education research as well as clinical research, Prof. Dr. Manfred Spitzer - one of the best-known neuroscientists in Germany - argues that digital media usage has a considerable negative impact on mental functioning, which is caused by detrimental effects on education and health. His book on the topic has spurred a massive public debate in Germany.

Pathogenic mechanisms of this include "outsourcing" mental work from our brains to machines and replacing face-to-face with digital contact, resulting in decreased empathy towards parents and peers. The proliferation of digital technologies is also responsible for a greater number of distractions, such as multitasking and incessant Internet use, resulting in dysfunctional attention and thought processes. Furthermore, by surrendering control of our lives to gadgets, we are knowingly increasing chronic stress, which is known to have a negative impact on physical and mental functioning. Likewise, digital media use can cause a plethora of issues, including addiction, anxiety, sleeplessness, depression, hypertension, obesity, personality disorders, increased aggression, dissatisfaction with life and loneliness as well as lack of exercise and recreational outdoor activities.

As depicted in this figure, the sum of the capabilities of the human brain increases during its development within the first two decades of life. During this time, the brain achieves its functions by the continuous processing of information. Unlike a computer, the brain contains neither a central processing unit (CPU) nor a storage device, such as a hard drive, but rather consists of approximately 100 billion neurons with roughly 10,000 connections each. These connections change in strength upon their use.

The overuse of digital media impairs brain development to its full capacity, leading to lower intellectual achievement and health as well as to an earlier onset of mental decline. Prof. Dr. Spitzer calls this phenomenon "digital dementia." Needless to say, Prof. Dr. Spitzer is not against the use of digital information technology per se. But he cautions against the unrestricted, market-driven exposure of society's most precious resource: the minds of the next generation.

Source: Manfred Spitzer, MD, PhD, Professor and Chairman, Department of Psychiatry, Transfer Center for Neurosciences and Learning (ZNL), University of Ulm


Alzheimer's patients frequently suffer from sleep disorders, usually even before they become forgetful. It is also a well-known fact that sleep plays a very important role in memory formation. 

Alzheimer�s disease (AD) is one of the great challenges in medicine today with no treatments currently available to delay, slow, or prevent the disease. AD is characterized by the accumulation of plaques consisting of toxic amyloid-beta peptides, which are located in the brain. However, the mechanisms by which these plaques disrupt memory and other cognitive functions are still unknown.

In recent years, there has been an increased focus in Alzheimer�s research on impairments of the sleep-wake cycle for several reasons: First, sleep problems are common in AD even in the absence of cognitive symptoms. Second, sleep is critical to cognitive functions, in particular, to learning and memory. Third, the buildup of plaques in the brain is directly modulated by the sleep-wake cycle, with toxic amyloid beta peptides being cleared from the brain during sleep. How impaired sleep, amyloid plaques, and memory failure are linked in AD, however, has remained unclear.

At the Technical University of Munich, new research in mice that are genetically predisposed to develop amyloid plaques in the brain demonstrates that the accumulation of plaques impairs a particular brain rhythm during sleep. These so-called slow-wave oscillations are required for the long-term consolidation of new memories.

The German researchers discovered that the impairment of the sleep-slow oscillations is due to an abnormal overactivity of neural networks in the cerebral cortex. Giving the mice a very low dose of a benzodiazepine - a class of sleep-inducing drugs - reduced the overactivity, relieved the animals of their sleep deficits, and improved their learning and memory abilities.

The results of this research reveal a novel mechanism that could underlie memory deficits in Alzheimer�s disease. Targeting abnormal sleep-slow oscillations may improve memory impairments in Alzheimer�s patients, which will be very important to explore further in the future.
Image: Neurons and plaques imaged with two-photon microscopy.

Source & Image: Marc Aurel Busche, MD, PhD, Department of Psychiatry and Psychotherapy, Institute of Neuroscience &
Munich Cluster for Systems Neurology (SyNergy), Technical University of Munich


In today's age of information overload, learning and retaining new information can be challenging. It can also be difficult to know where to start and how to incorporate the practice of studying into one's busy schedule.
Semper - a mobile "micro-learning" app - helps integrate learning into one's daily routine by breaking down new information into bite-sized pieces. The brain training app uses natural breaks in a user's flow - e.g. when unlocking his or her smartphone screen or opening another app - to deliver short learning opportunities. Roughly three to five seconds in length, these learning opportunities are spread out over the course of the day and support the observation that learning is most effective when done in numerous short sessions.

Rather than having to set aside a specific time to study, Semper effortlessly integrates learning into one's life. The app's algorithm learns from an individual user's answer patterns to ensure that questions are matched to the user's specific aptitudes. The start-up has also created a community-driven content marketplace that enables users to create, upload, and share personalized learning materials.

The University of Potsdam in Germany ran a study analyzing the effectiveness of Semper. The study examined more than three million responses to math questions and found that users' performance - including accuracy and speed - doubled over a two-week period.

Semper was founded by Berlin-based entrepreneurs Felix Nienst�dt and Simon Smend under the former company name UnlockYourBrain. The app has already been downloaded over 500,000 times and is used an average of two million times per day. Semper works with a variety of partners, including MINT Zukunft Schaffen, Stiftung Rechnen, and Telekom Topapps.

Source & Image: UnlockYourBrain GmbH   

As the founding director of Network Aging Research (NAR) at Heidelberg University, Prof. Dr. Konrad Beyreuther has been extremely active in bringing together humanistic and scientific aging research. The network unites the research activities of the Universities of Heidelberg and Mannheim as well as numerous other research institutions in the Rhine-Neckar area.
Until his appointment at NAR, Prof. Dr. Beyreuther was head of a laboratory that conducted research on the genetics, molecular and cellular biology of neurodegenerative disorders. His aim was to unravel the physiological and pathogenic function of key genes and mechanisms that underlie and drive the processes causing dementia. Internationally recognized for his work on Alzheimer's and on the key gene involved in the development of the disease, Prof. Dr. Beyreuther was awarded the honorary title of Senior Professor by the rector of Heidelberg University.
In his interview with GCRI, Prof. Dr. Beyreuther discusses what occurs in the brain of an Alzheimer's patient and how Alzheimer's disease is diagnosed. He addresses the importance of early diagnosis and also shares his thoughts on how far he thinks we are from finding a cure. To read the full interview, click here.
Prof. Dr. Beyreuther received his doctorate in 1968 from the Max Planck Institute of Biochemistry in Munich. He completed research training at Harvard and at the MRC Laboratory of Molecular Biology in Cambridge, England, as well as postdoctoral work at the Institute for Genetics at the University of Cologne. In 1987 he accepted a professorship at the Center for Molecular Biology (ZMBH) at Heidelberg University, which he held until 2007. He has been awarded numerous accolades for his accomplishments in scientific research and university teaching, including the prestigious Officer's Cross of the Order of Merit of the Federal Republic of Germany (Bundesverdienstkreuz der Bundesrepublik Deutschland), the Lennox K. Black International Prize for Excellence in Medicine, and the Henry M. Wisniewski Award for Lifetime Achievement in Alzheimer's Disease Research.

Source & Image: Heidelberg University

Imagine if you could determine your risk for developing Alzheimer's based on how you navigate a virtual maze. As it turns out, a team of German and Dutch neuroscientists has conducted research on this very concept.
Their findings published in Science indicate that young adults with a genetically increased risk for Alzheimer's have altered activation patterns in a brain region that is crucial for spatial navigation. This research was headed by Prof. Dr. Nikolai Axmacher, formerly at the German Center for Neurodegenerative Diseases in Bonn, who is now working at the Ruhr-Universit�t Bochum.

The researchers recruited two groups of young adults aged 18-30 to navigate a virtual setting - one group with the e4 variant of the APOE gene, the largest genetic risk factor for developing Alzheimer's later in life, and the other group without. Interestingly, the at-risk group performed just as well on the test as their peers, but navigated the maze differently and had reduced functioning of a type of brain cell involved in spatial navigation.

One of the areas affected by Alzheimer's disease at an early stage is the entorhinal cortex. This region of the brain is crucial for navigation and contains "grid cells" that fire in a spatial grid pattern. In 2010, Prof. Dr. Christian Doeller, presently at Radboud University in Nijmegen, demonstrated that the grid cell system in humans can be recorded indirectly using functional magnetic resonance imaging when subjects navigate a virtual environment.

Prof. Dr. Axmacher and his colleagues, including graduate student Lukas Kunz, analyzed the grid cell system in the entorhinal cortex of the two groups of students. "The risk carriers showed a less stable grid pattern - many decades before they might develop Alzheimer's dementia," Lukas Kunz said. Moreover, risk carriers moved less frequently in the center of the virtual landscape, which indicates an altered navigation strategy. In the risk group, the brain activity in the memory system was also generally increased.

While these findings can't predict whether at-risk people in the study will develop Alzheimer's later in life, they may provide key insights into why some people are more susceptible to the disease.

Source: Dr. Marcus Neitzert, German Center for Neurodegenerative Diseases (DZNE)

Image: Bureau BlauwGeel 

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