Can memory partially recover in Alzheimer's disease?
A new review study from Magdeburg shows that disruptions in brain networks play a greater role than previously thought and could be specifically targeted.
Memory loss in Alzheimer's disease is not caused solely by the loss of nerve cells. Disrupted processes in the brain's networks also play an important role. This is the conclusion of a recent review article in the journal Nature Reviews Neurology by researchers from the Institute for Cognitive Neurology and Dementia Research at Otto von Guericke University Magdeburg, the German Center for Neurodegenerative Diseases (DZNE), and the Leibniz Institute for Neurobiology Magdeburg (LIN). The study opens up new perspectives for the diagnosis and treatment of the disease.
Memory as the Interaction of Brain Networks
Memories arise through the coordinated interaction of several brain regions. This network, which includes the hippocampus as well as areas in the frontal and temporal lobes, enables what is known as episodic memory—that is, the recollection of personal experiences.
In Alzheimer’s disease, pathological changes spread along these connections and disrupt communication within the network. Typical consequences include difficulty retrieving memories, confusing experiences, and problems learning new information.
“In the brain, memory is organized into distinct circuits,” explains Prof. Dr. Emrah Düzel, Director of the Institute for Cognitive Neurology and Dementia Research Magdeburg and Site Director of the DZNE in Magdeburg. “When these circuits no longer work together efficiently, memory problems arise—even if parts of the structure are still intact.”

Photo: As a neurologist, Prof. Dr. Emrah Düzel studies how episodic memory is organized in the brain, how it is regulated by neurotransmitters, and how it changes with age or in the context of neurodegenerative diseases—as well as the adaptability of these networks. Photographer: Sarah Kossmann/Magdeburg University Medical Center
Focus on the Use of Existing Resources
A central concept of the research is the so-called “Circuit Utilization Framework.” It describes how not only the structural state of the brain is crucial, but also how well existing networks are utilized. According to this framework, some memory impairments could be attributed to the fact that existing connections are no longer optimally activated or coordinated.
“We see evidence that functional capacities still preserved in the brain can no longer be reliably utilized,” says the neuroscientist. “This opens up the possibility of specifically targeting the functioning of these networks and circuits.”
About 80 percent of people with Alzheimer’s disease are affected by the amnestic form, in which episodic memory is particularly impaired. Differences in disease progression could be explained, among other things, by the brain’s ability to compensate for deficits (cognitive reserve).
Observations show that some people exhibit only mild symptoms for a long time despite detectable Alzheimer’s changes. Others develop significant memory problems early on. Factors such as education, mental activity, and life experience may play a role in this.
“The brain has more capabilities than we long thought,” says co-author Hon. Prof. Michael Kreutz, head of the Neuroplasticity Research Group at the LIN in Magdeburg. “It can take detours. But we are only beginning to understand how we can specifically promote this process.”

Photo: Honorary Professor Dr. Michael Kreutz has been studying the molecular basis of memory and learning for decades—in particular, the biological mechanisms at synapses that are crucial for information storage in the brain. Photographer: Sarah Kossmann/Magdeburg University Medical Center
New Approaches for Therapy and Diagnostics
The findings of this research suggest that therapies should be more strongly oriented toward the function of brain networks. These include, among other things:
- Targeted memory training that strengthens specific cognitive processes
- Stimulation of brain regions, for example through electrical or magnetic methods
- Medications that regulate the activity of nerve cells.
Initial clinical studies show that measurable improvements in memory performance can be achieved through the targeted modulation of specific brain regions—particularly in the hippocampus. These effects have so far been observed primarily in early stages of the disease. “We need to make better clinical use of this knowledge,” says Prof. Düzel. “It is time to examine memory problems in Alzheimer’s at the level of neural circuits and computational processes. This will allow us to better understand which processes in the brain are disrupted and to develop and implement more targeted interventions. In the future, we must treat Alzheimer’s disease both causally, e.g., with anti-amyloid antibodies, and mobilize and strengthen the brain’s remaining resources.”
Perspectives for Research and Care
The current study summarizes existing research findings and uses them to describe a new explanatory model. It is based on data from various studies—including patient studies, imaging techniques, and experimental work.
Other research groups are pursuing similar approaches. However, there are some differences in estimates regarding the actual proportion of reversible functional impairments. It is undisputed that structural damage—that is, the loss of nerve cells—cannot be reversed with current knowledge. This highlights the need to implement therapeutic approaches as early as possible in the course of the disease.
Further clinical studies are needed to determine whether and to what extent memory function can be improved in everyday life as a result. Questions regarding the costs and availability of such treatments also remain unanswered. Many of the procedures currently under investigation are being developed and funded within the framework of clinical trials.
In the long term, this approach could help to better understand the course of the disease and maintain the quality of life of those affected for longer.
This work was supported by the German Research Foundation (DFG) as part of the Collaborative Research Center Neural Resources of Cognition SFB1436 at the Otto von Guericke University Magdeburg as well as by the German Center for Neurodegenerative Diseases (DZNE).
Original publication
Düzel, E., Kreutz, M.R. Maintaining and regaining episodic memory in Alzheimer disease: a circuit-based perspective. Nat Rev Neurol (2026). https://doi.org/10.1038/s41582-026-01189-9
Scientific Contacts
Prof. Dr. med. Emrah Düzel, Director of the Institute for Cognitive Neurology and Dementia Research at Otto von Guericke University Magdeburg, emrah.duezel@med.ovgu.de; Tel.: +49 (0)391/ 67 25050
Prof. Dr. rer. nat. Michael R. Kreutz, Honorary Professor of Molecular and Cellular Neuroscience at Otto von Guericke University Magdeburg and Head of the Neuroplasticity Research Group at the Leibniz Institute for Neurobiology Magdeburg, Michael.Kreutz@lin-magdeburg.de
