Alzheimer’s: Treating forgetfulness with a brain pacemaker

Success with correct image interpretation

Horn and his team have specialized in analyzing high-resolution images of the brain that are recorded using magnetic resonance imaging and, in combination with computer models, in precisely detecting the optimal stimulation points for DBS in the brain. “A particular challenge here is that every brain is different. And that plays a major role in the implantation of the electrodes,” the expert was quoted as saying in a broadcast from the university clinic. “If you’re just a few millimeters off, the expected effect may not be there.”

This was also the case for the majority of the 46 study participants with Alzheimer’s disease. However, in those patients in whom DBS showed a positive effect, the target structure for the electrodes might finally be pinpointed. “It lies at a branch point between two nerve fiber bundles – the fornix and the stria terminalis – that connect deep brain regions. Both structures are associated with memory function,” explained the neuroscientist.

Further studies necessary

Further clinical studies are required before DBS can be approved and used for the treatment of Alzheimer’s disease. But with the data for the precise implantation of the electrode, there is a basis for further clinical studies. “If our data helps to place the electrodes more precisely in neurosurgical studies testing DBS in Alzheimer’s, that would be great,” said Horn. “Because we urgently need an effective and symptom-relieving therapy for Alzheimer’s in order to be able to help the patients – DBS is a promising approach for this.”

Treatment costs worldwide enormous

Around 55 million people worldwide suffered from dementia in 2019, most of them from Alzheimer’s disease. The numbers are constantly increasing due to age development. The costs due to such diseases have been calculated at more than 800 billion euros per year. The drugs used to date for Alzheimer’s disease, for example the so-called cholinesterase inhibitors, only have a relatively weak effect on the symptoms. Causal therapies aim to eliminate harmful deposits of the proteins beta-amyloid or tau. Monoclonal antibodies, such as lecanemab, are to be used once morest beta-amyloid. However, many such projects have failed so far. In the recent past, this has also led to considerable doubts as to whether beta-amyloid or tau proteins are really causally related to Alzheimer’s dementia.

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