Forschungszentrum Jülich GmbH
Institute of Biological Information Processing: Structural Biochemistry (IBI-7)
Dr. Janine Kutzsche, is working in the field of neurodegenerative diseases, is team leader of the working group AD-therapy since 2013 at the Institute of Biological Information Processing at the Forschungszentrum Jülich. She is responsible for the organization and monitoring of the scientific research with regard to drug development.

Moderator of 1 Session

Session Type
SYMPOSIUM
Date
Wed, 16.03.2022
Session Time
04:15 PM - 06:00 PM
Room
ONSITE: 131-132

Presenter of 1 Presentation

AΒETA OLIGOMER ELIMINATION IMPROVES COGNITION IN AGED BEAGLE DOGS - A MODEL OF SPORADIC ALZHEIMER’S DISEASE.

Session Type
SYMPOSIUM
Date
Wed, 16.03.2022
Session Time
04:15 PM - 06:00 PM
Room
ONSITE: 131-132
Lecture Time
05:15 PM - 05:30 PM

Abstract

Aims

Alzheimer´s Disease (AD) currently affects more than 24 million people worldwide, but to date, no curative or disease modifying treatment exists. During the last years, our group developed a drug candidate named RD2, which directly disassembles and destroys toxic Aβ oligomers, the Aβ species postulated to be responsible for the development and progression of AD. The aim of this study was to investigate the treatment efficacy of RD2 with regard to cognition and biomarkers in aged beagle dog - a model of sporadic AD -.

Methods

Aged beagle dogs were treated orally for three months with low or high doses of RD2 or placebo. Behavioral assessments were conducted longitudinally and CSF and plasma samples were collected at baseline and every month during the treatment period and during an additional two months after treatment discontinuation.

Results

Only RD2 treated dogs showed a significantly improved cognitive performance compared to baseline, even after the wash out period of two months.

Conclusions

We were able to show that RD2 significantly improves cognitive deficits in aged Beagle dogs. The maintenance of the cognitive improvement during the washout period even suggests a neuroprotective and truly disease-modifying effect of RD2.

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