Alzheimer's culprit causes memory loss even before brain degeneration

May 29, 2015, University of Sussex
Diagram of the brain of a person with Alzheimer's Disease. Credit: Wikipedia/public domain.

The study, published May 29 in the open access Nature Publishing Group journal Scientific Reports, reveals a direct link between the main culprit of Alzheimer's disease and memory loss.

Alzheimer's disease is characterized by the formation of in the . These amyloid plaques are made up of an insoluble protein, 'Amyloid-beta' (Abeta), which forms small structures called 'oligomers' that are important in the disease progression.

Although these proteins are known to be involved in Alzheimer's, little is understood about how they lead to memory loss.

Sussex Neuroscience researchers investigated how Abeta affected healthy brains of pond snails (Lymnaea stagnalis) by observing the effect of administering the protein following a food-reward training task.

The results showed that snails treated with Abeta had significantly impaired memories 24 hours later when tested with the food task, even though their brain tissue showed no sign of damage.

Lead author on the study Lenzie Ford said this demonstrated that Abeta alone is enough to lead to the symptoms of memory loss that are well known in Alzheimer's disease.

She said, 'what we observed was that snail brains remained apparently healthy even after the application of the protein. There was no loss of brain tissue, no signs of cell death, no changes in the normal behaviour of the animals, and yet memory was lost.

'This shows that Alzheimer's don't just affect memory by killing neurons of the brain, they seem to be targeting specific molecular pathways necessary for memories to be preserved.'

Professor George Kemenes, a Sussex neuroscientist who pioneered a thorough understanding of the molecular mechanisms of learning and memory in the pond snail's nervous system, said, 'because we understand the memory pathways so well, the simple snail brain has provided the ideal model system to enable us to link the loss of established memory to pure Abeta'.

The work will provide a platform for a more thorough investigation of the mechanisms and effects on pathways that lead to this .

Professor Serpell, a senior author on the study and co-director of the University of Sussex's Dementia Research Group, said, 'It is absolutely essential that we understand how Alzheimer's disease develops in order to find specific targets for therapeutics to combat this disease.'

Explore further: Scientists use immunotherapy to reduce memory problems with Alzheimer's disease

More information: 'Effects of Aß exposure on long-term associative memory and its neuronal mechanisms in a defined neuronal network' Ford, L., Crossley, M., Williams, T., Thorpe, J.R., Serpell, L.C., Kemenes, G. Sci. Rep. 5, 10614; DOI: 10.1038/srep10614 (2015).

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3 comments

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Jim4321
not rated yet May 29, 2015
This is a very interesting result. It focuses attention on the question: "What causes Alzheimer's?" Is Alzheimer's provoked by abeta, by a malfunction of tau or by something else? What factor is the first cause in the chain of disfunction?
yvchawla
May 29, 2015
This comment has been removed by a moderator.
Jim4321
5 / 5 (1) May 29, 2015
@yvchawla Do you know any 150 year old people? Both Bhudda on the one hand and Sri Maharshi on the other have died. Both of them knew the One. Perhaps you have causation reversed and mental and physical decay lead to complacency about the 1000 things etc.

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