Maryland: For the first time, scientists have found a link between high levels of glucose in the brain and the symptoms of Alzheimer's disease.
Our brains break down glucose sugar in its most basic form to provide energy to make our higher work.
People whose brains were worse at breaking down glucose suffered more brain plaques and tangles, the hallmark of the disease.
Also, people whose brains were less efficient at breaking down glucose suffered worse outward dementia symptoms such as memory loss associated with Alzheimer's disease.
While the research is only at an early stage, and it is not clear why being bad at breaking down glucose causes plaques and tangles.
Dr. Madhav Thambisetty, at the National Institute of Aging in the US, looked at brain tissue samples from autopsies collected by the Baltimore Longitudinal Study on Aging, part of a research project which tracks the health conditions of people over several decades.
Dr. Thambisetty and colleagues focused on brain areas that are vulnerable to plaques and tangles the frontal and temporal cortex highly involved in memory and language.
They also looked at areas which resist these features, such as the cerebellum which deals with movement, muscles and muscular activity.
They found that the people with more severe Alzheimer's had problems breaking down the glucose to produce energy a process known as glycolysis.
A slower rate of glycolysis and higher brain glucose levels was associated with more severe plaques and tangles in the brains of people with the disease.
Worse brain glycolysis was also related to Alzheimer's symptoms such as memory problems.
Richard J Hodes of the NIA said: 'For some time, researchers have thought about the possible links between how the brain processes glucose and Alzheimer's.
'Research such as this involves new thinking about how to investigate these connections in the intensifying search for better and more effective ways to treat or prevent Alzheimer's disease.'
The researchers also found that people with Alzheimer's had lower levels of enzymes used to break down glucose, and lower levels of a protein called GLUT-3 that transports glucose in brain cells and the lower the levels of GLUT-3, the worse the plaques and tangles were.
In addition, they found that people with higher blood sugar levels in the years before they died were linked to greater levels of glucose in the brain when they died.
Dr. Thambisetty said: 'These findings point to a novel mechanism that could be targeted in the development of new treatments to help the brain overcome glycolysis defects in Alzheimer's disease.'
He added the study did not test directly whether eating high levels of sugar might be a bad idea to people who are less able to process glucose.
'Thus, while we found significant abnormalities in glucose breakdown in the brains of patients with Alzheimer's, the exact reasons for these abnormalities remain to be understood.
'This is a question that would need to be addressed in future studies and would be a direct extension of the findings we reported in the paper. There may be both genetic and environmental causes of these abnormalities, but they remain to be identified.'
Dr. Clare Walton, the research manager at Alzheimer’s Society, says: 'The link between how well the brain uses glucose and Alzheimer’s disease is not new – in fact, we’ve been using brain scans that show changes in glucose use to study the disease for more than 30 years.
'What we don’t know is whether changes in brain glucose metabolism play a role in causing or worsening Alzheimer’s disease or whether the changes are just a by-product of damage already occurring in brain cells.
'This innovative research looks at glucose metabolism in a new way – by examining the brain tissue of people who have died – and suggests that changes in the pathways that transport and use glucose in the brain cells occur as Alzheimer’s disease progresses.
'As these changes appear to precede the onset of dementia symptoms, they should be further investigated.'
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