Synaptic Tau Oligomers in Alzheimer’s Disease – A Possible Culprit in the Spread of Tau Pathology throughout the Brain
Alzheimer’s disease is considered one of the most common causes of dementia in older individuals. Among the neuropathological features of Alzheimer’s disease (AD), the synaptic loss is the primary correlate of cognitive decline, and the progression of tau pathology in the brain of AD is closely correlated with synaptic loss and cognitive symptoms.
A collaborative study between the Memory Unit, led by Prof. Tara Spires-Jones at the University of Edinburgh, and the group led by Dr Sílvia Pujals from IQAQ-CSIC, has been published in the journal Neuron, providing key insights into the spread of harmful proteins that accumulate in the brains of individuals with Alzheimer’s disease.
What did we do in this study?
In this study, over 1 million synapses were examined in samples from different brain regions of 42 donor individuals using novel super-resolution microscopy techniques that allow visualization of proteins within individual synapses.
This work has discovered that small accumulations of the tau protein, known as tau oligomers, are present within synapses in individuals who died from Alzheimer’s disease. Tau oligomers were observed within both sides of the synapse, from the signalling-sending brain cell to the signalling-receiving brain cell. This study indicates that synapses have the capacity to transmit toxic forms of tau protein from one part of the brain to another. These findings reinforce that halting the spread of toxic tau is a promising strategy for treating the disease.