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Brain Fights Forgetfulness

When thought process cease to work smoothly, the brain appears to develop new communication strategies. Brain regions not strongly associated with the task at hand step up their cooperation. Internal processes within one part of the brain and involved in the task are also boosted. The human brain uses this trick to continue functioning in an optimal manner. In this way, the brain may stave off the devastating effects of the deterioration process occurring in diseases such as Alzheimer’s. These are the findings of a new study performed by Jülich researcher Dr. Heidi Jacobs based on investigations she conducted at Maastricht University. The results will appear on 31 January 2012 in the renowned journal Neurology.

For the study, Dr. Jacobs asked 18 healthy volunteers and 18 patients with incipient Alzheimer’s disease to perform a mental rotation task. Her test persons were asked to identify whether two three-dimensional structures displayed next to each other were congruent or incongruent. During the task, Dr. Jacobs used magnetic resonance imaging to register the brain activity of the participants. Her amazing results: despite the incipient dementia, the patients with Alzheimer’s performed just as well and as quickly as the healthy controls.

However, the activity of the brain regions involved showed clear differences. The researchers observed changes in the patients with Alzheimer’s in the parietal lobe – a brain region in the upper back part of the head. The parietal lobe is strongly connected with the medial temporal areas, which are important for memory. “The parietal lobe is involved in numerous mental abilities,” Dr. Jacobs explains, “for example, for doing mathematics, for paying attention, for episodic memory or explicit memory, for spatial relationships between objects and even for meditation. Areas within the parietal lobe appear to collaborate more with each other, possibly to maintain cognitive performance” Dr. Jacobs points out. “However, important functional collaborations with other central brain regions appear to be disturbed in the patients with Alzheimer’s.” The impaired regions primarily involve the areas that are part of a central memory network. “Decline in memory performance is one of the key deficits associated with Alzheimer’s disease,” Dr. Jacobs says.

The neuropsychologist and her team assume that the patient’s brain is able to use the altered communication pathways to compensate for deficiencies in other places. When and how the brain ultimately loses the race between deterioration and compensatory mechanisms in patients with severe dementia is a fascinating question for the researchers. “We would like to know how this amazing reorganizational capacity – in particular in the parietal lobe – changes during the course of the disease, especially in the stages in which the patients convert from having cognitive deficits to manifesting Alzheimer’s disease.”

Consequently, they hope to better understand the disease mechanisms of dementia disorders such as Alzheimer’s disease. At the same time, the scientists are exploring new therapeutic approaches. “Targeted neurostimulation or drugs could positively reinforce these compensatory processes in the brain in future – which might conserve mental abilities longer,” Dr. Jacobs points out. Together with her colleagues at Forschungszentrum Jülich’s Institute of Neuroscience and Medicine in the Cognitive Neurology department headed by Prof. Gereon R. Fink, she hopes to achieve this and more. “At the same time, we are seeking a biomarker that would indicate these compensatory processes and would allow us to identify incipient dementia much earlier and, ideally, permit us to delay it,” says Dr. Jacobs, describing her vision of the future.

Original publication:
Functional integration of parietal lobe activity in early Alzheimer disease
H.I.L. Jacobs, PhD, M.P.J. Van Boxtel, MD, PhD, A. Heinecke, MSc, E.H.B.M. Gronenschild, PhD, W.H. Backes, PhD, I.H.G.B. Ramakers, PhD, J. Jolles, PhD and F.R.J. Verhey, MD, PhD
Neurology WNL.0b013e318245287d;
DOI: 10.1212/WNL.0b013e318245287d

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