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Healthy brain networks
Image by Gerd Altmann from Pixabay

The study, led by scientists at the University of Cambridge, demonstrates that build-up of the ‘toxic’ brain protein Tau – linked with the onset of Alzheimer’s disease – is accompanied by impairments to the brain’s neurophysiology.

The research made use of non-invasive magnetoencephalography (MEG) and electroencephalography (EEG) brain scans taken from participants with probable early Alzheimer’s disease in the pilot phase of the DPUK-led Deep and Frequent Phenotyping study.

First author Dr Ece Kocagoncu, of Cambridge’s Department of Clinical Neurosciences, said: ‘We urgently need to find new ways to detect Alzheimer’s disease earlier, and critical to this is understanding the role that Tau has in early neurophysiological changes that occur in the brain.

‘In this study we looked at the relationship between Tau accumulation in the brain and how that affects our neurophysiological brain networks, or the way the brain’s nerve cells talk to each other. Alzheimer’s studies generally use techniques like MR or PET scanning to produce images of the brain based on blood oxygenation or glucose levels, but we wanted to use MEG and EEG to measure directly the electrical and magnetic fields generated by the brain’s neuronal activity.’

The research used four measures to test the effect of Tau build-up on the brain’s neurophysiology. Two of those measures looked at the efficiency of information transfer at a local and global level respectively, while the other two looked at ‘hubness’ – that is, the extent to which a particular region of the brain acts as a focal point for information transfer – and diversity of functional connections in brain regions.

Dr Kocagoncu, who also works on the Cambridge-based, DPUK-funded New Therapeutics in Alzheimer’s Disease (NTAD) study, said: ‘We used these four measures to help us understand how the development of Alzheimer’s disease changes the main characteristics of brain networks.

‘We found that as Tau increases in certain areas of the brain, the “hubness” of those areas decreases, which means the brain’s communication networks become more fragmented and less well connected as Alzheimer’s takes hold. We also found that increasing levels of Tau are accompanied by decreases in the efficiency of information transfer in the brain, meaning the brain works less optimally with Alzheimer’s disease.

‘Using MEG and EEG allowed us to look at frequency-specific information transfer in the brain. We found that in Alzheimer’s disease, the impairments in communication between nerve cells mostly take place in higher frequency bands.’

These preliminary findings provide evidence of neurophysiological network biomarkers in relation to Tau accumulation that may prove useful as non-invasive tools to track short-term Alzheimer’s progression and the impact of disease-modifying therapies on brain function.

The team will carry out the same research on data from participants in the full Deep and Frequent Phenotyping (DFP) study, which will collect information on a range of measures from 250 people at risk of Alzheimer’s around the UK.

For its size, DFP is the world’s most detailed study to date into preclinical Alzheimer’s disease. When completed, researchers will be able to use the data obtained through DFP to understand whether early interventions are working. DFP is funded by the MRC and NIHR.

Read the full study in the journal Neurobiology of Aging.