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Alzheimer′ s Disease

Alzheimer´s disease is a progressive, neurodegenerative disorder and the most common type of dementia. Currently more than 24 million people are affected worldwide. Our research focusses on developing methods for pre-symptomatic diagnosis and new therapeutic approaches.

Alzheimer´s disease (AD) is a progressive, neurodegenerative disorder, which is characterized by progressive memory deficits, cognitive impairments and personality changes. AD is the most common type of dementia (60%). Currently more than 24 million people are affected worldwide. It is estimated that this number will almost be doubled to 44 million by 2030. Age is the most important risk factor for AD. In the age group of 65 to 69, every 20th person suffers from dementia, but in the age group of 80 to 90 already every fourth person is affected. In addition to the immense distress of the patients and their families, the total estimated costs of AD are about US$ 600 billion with strongly increasing tendency, making it a major thread for our healthcare systems.

So far there is no causal therapy for AD. Currently only two medicinal products, i.e. acetylcholinesterase inhibitors and the NMDA receptor antagonist Memantin, are available, which only temporarily improve symptoms, but are not able to slow down, halt or even reverse disease progression. Due to this fact, researchers worldwide are currently working hard towards effective drugs. Another problem lies in the field of diagnostics: Currently, clinical diagnosis of Alzheimer´s disease is largely based on the assessment of symptoms through psychological and cognitive tests. However, this approach offers only limited accuracy and reliability. It also does not allow for early diagnosis in the presymptomatic stage.

A pathological hallmark of Alzheimer's disease is the deposition of amyloid plaques, which are present long before onset of clinical symptoms. Plaques consist mainly of amyloid-ß-peptides (Aβ). Aß is produced from the amyloid precursor protein (APP) by distinct proteolytic activities, called β- and γ-secretases. The resulting Aß monomers are not toxic per se, but they can form small soluble aggregates (oligomers) and amyloid fibrils. It is generally assumed that diffusible Aβ oligomers are the major toxic species responsible for disease development and progression.


Up to now, efforts have concentrated to reduce generation of Aß or reduce its concentration in order to decrease Aß aggregation. In our opinion, instead of Aß monomers the Aß oligomers should be the target of any treatment. Thus, we focus on the development drugs that are able to destroy toxic Aß oligomers. Additionally, Aß oligomers or aggregates could be exploited as early biomarkers for AD, which are urgently needed for measuring therapeutic effects of drug candidates.

The Bannach group is developing an ultra-sensitive and quantitative method for early and pre-symptomatic diagnosis of AD, via detection and quantitation of Aß aggregates in liquor and blood.

The Kutzsche group is pursuing and developing new therapeutic approaches for the treatment of AD.

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