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Content archived on 2023-03-06

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Missing link between Alzheimer's and epilepsy found

Researchers have discovered a protein link between Alzheimer's disease and epilepsy. Published in the Journal of Neuroscience, the research is the first major finding of the EU-funded MEMOLOAD ('Neurobiological mechanisms of memory loss in Alzheimer's disease') project and wil...

Researchers have discovered a protein link between Alzheimer's disease and epilepsy. Published in the Journal of Neuroscience, the research is the first major finding of the EU-funded MEMOLOAD ('Neurobiological mechanisms of memory loss in Alzheimer's disease') project and will shed light on how to improve treatment for both diseases. MEMOLOAD is funded under the Health theme of the Seventh Framework Programme (FP7) to the tune of EUR 3 million. 'We have shown for the first time the actual cellular process that links epilepsy and Alzheimer's disease,' highlighted Dr Tibor Harkany from the University of Aberdeen in the UK. 'Our findings could lead to a rethink of the type of drugs given to patients.' According to Dr Harkany, a number of drugs used to treat memory loss have the potential to lower a patient's seizure threshold, while anti-epileptic drugs can further weaken the cognitive functions of Alzheimer's sufferers. 'It may be that we need to look for new drugs that treat both diseases at the same time,' the co-author of the paper said. Researchers were already aware that the chemical beta-amyloid impacts on the cognitive abilities of Alzheimer's sufferers, who can experience epileptic seizures. Past studies have shown that epileptic seizures can affect around a third of Alzheimer's patients, but why seizures occur remained a mystery. It should be noted that people suffering from certain forms of the disease are 80 times more likely to have seizures compared with people without the condition. This latest work discovered that beta-amyloid triggers more excitable and sensitive nerve cells. This impact obstructs communication between the cells and sets off seizures. The researchers performed video-EEG (electroencephalogram) recordings in mice carrying mutant human APPswe (mutant amyloid precursor protein) and PS1dE9 (mutant presenilin 1) genes and their wild-type littermates (i.e. non-transgenic littermates) to determine the prevalence of unprovoked seizures. 'An electrographic seizure was defined as high-amplitude rhythmic discharges that clearly represented a new pattern of tracing (repetitive spikes, spike-and-wave discharges, slow waves) and lasted for equal to or greater than five seconds,' the authors wrote in the paper. 'In two recording episodes at the onset of beta amyloid pathogenesis, at least one unprovoked seizure was detected in 65% of APdE9 mice [mice carrying APPswe and PS1dE9], of which 46% had multiple seizures and 38% had a generalised seizure.' No wild-type mice suffered seizures. The finding 'explains some of the link between Alzheimer's and epilepsy, adding a piece to the puzzle of what is happening in the brain during dementia', said Rebecca Wood, head of the Alzheimer's Research Trust in the UK, one of the funding bodies. 'By understanding what is happening in the brain, researchers can work towards effective treatments that are so desperately needed by the 700 000 people in the UK with dementia.' Launched in 2008, MEMOLOAD is investigating the molecular mechanisms behind memory loss in Alzheimer's disease. The partners believe the project's results will fuel understanding of brain memory mechanisms at the behavioural network, synaptic and molecular levels of dysfunction in Alzheimer's disease.

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