Sam Lister, Health Editor
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Insulin, the hormone that regulates levels of sugar in the blood, may slow or prevent memory loss caused by Alzheimer’s disease, a study suggests.
Researchers examining the effects of diabetes drugs on the brain have found that the medication appears to protect cells responsible for the formation of memory.
The work offers further support for the theory that Alzheimer’s could be caused by a form of diabetes linked to the body’s failure to produce and process insulin effectively.
It raises hopes of the development of new treatments for Alzheimer’s, which is incurable and is characterised by progressive memory loss and mental decline. About 700,000 people in Britain have dementia, with most suffering from Alzheimer’s.
The latest study, published in the Proceedings of the National Academy of Sciences, concludes that insulin may slow or prevent the memory loss caused by toxic proteins which attack the brains of Alzheimer’s sufferers.
The team of researchers from Northwestern University in Illinois and the Federal University of Rio de Janeiro in Brazil carried out a study that involved treating neurons taken from one of the brain’s memory centres – the hippocampus – with insulin and the diabetes drug rosiglitazone.
Cells in the hippocampus are susceptible to damage caused by amyloid beta-derived diffusible ligands (ADDLs), toxic proteins that build up in people with Alzheimer’s.
ADDLs attack the synapses – the junctions between nerve cells through which impulses pass – which help form memory. After the proteins have attached, the synapses lose their capacity to respond to incoming information, resulting in memory loss.
The researchers discovered that damage to neurons exposed to ADDLs was blocked by insulin, which stopped the proteins from attaching to the cells. The insulin-sensitising drug rosiglitazone enhanced protection afforded by low levels of insulin, the study showed.
William Klein, a professor of neurobiology and physiology at the Weinberg College of Arts and Sciences and a researcher in Northwestern University’s Cognitive Neurology and Alzheimer’s Disease Centre, said: “Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer’s disease.
“Sensitivity to insulin can decline with ageing, which presents a novel risk factor for Alzheimer’s disease. Our results demonstrate that bolstering insulin signalling can protect neurons from harm.”
Fernanda De Felice, lead author and an associate professor at the Federal University of Rio de Janeiro, Brazil, said: “The discovery that anti-diabetic drugs shield synapses against ADDLs offers new hope for fighting memory loss in Alzheimer’s disease.”
Sergio Ferreira, another member of the research team and a professor of biochemistry in Rio de Janeiro, added: “Recognising that Alzheimer’s disease is a type of brain diabetes points the way to novel discoveries that may finally result in disease-modifying treatments for this devastating disease.”
The findings were welcomed by campaigners in the UK. Rebecca Wood, chief executive of the Alzheimer’s Research Trust, said it was known that diabetics were at a higher risk of developing Alzheimer’s and the study reinforced the link between insulin and brain function.
“The study sheds light on how insulin interacts with amyloid, a toxic protein found in Alzheimer’s. The most exciting implications are that some diabetes drugs have the potential to be developed as Alzheimer’s treatments," she said.
Ms Wood said that the Alzheimer’s Research Trust was also funding work looking at how insulin acts on the brain, which it hopes will lead to new treatments.
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