Spanish researchers discover a key step in the spread of Alzheimer’s | The USA Print

A study co-led by researchers from the group of Neurobiology of Dementias of the Research Institute of Hospital of Santa Creu i Sant Pau – IIB Sant Pau who publishes the neuron magazine of the Cell group, describes that the harmful proteins that accumulate in the brains of people with Alzheimer disease they propagate through the synapse.

The work, directed by the teacher’s team Tara Spiers-Jones, of the Dementia Research Institute of the United Kingdom at the University of Edinburgh, and carried out by the IIB Sant Pau in collaboration with the Institut de Química Avançada de Catalunya (IQAC) of the Superior Council of Scientific Investigations (CSIC), contributes new evidence that could be the key to stop progress Alzheimer’s.

The study was carried out within the framework of European project COEN, financed by Ciberned and coordinated by AAlberto Lleo, researcher in the Neurobiology of Dementias group at the IIB Sant Pau.

The accumulation of tau protein in neurons in form of neurofibrillary tangles It is one of the most characteristic aspects of Alzheimer’s. Deposits of this protein spread throughout the brain circuits and as they spread, disrupt communication between brain cells which leads to an alteration of brain functions. It is the first time that it can be observed, in human brains, how these abnormal shapes They spread through the brain through synapses.

What is the synapse?

The synapse are the connection points between brain cells that allow the flow chemical and electrical messages. This process is vital for normal brain function. Synapses are lost in Alzheimer’s disease and the loss of these connections strongly predicts the Loss of memory and other intellectual functions in these patients.

The research team examined more than a million synapses from 42 people by means of novel techniques carried out with high-power, super-resolution microscopes in collaboration with the IQAC-CSIC, which allowed visualizing the protein flow within individual synapses. The researchers were able to observe that small deposits of tau protein, Known as oligomers, they were on both sides of synapses in people who died of Alzheimer’s. That is, both in the neuron that sends signals as well as the one that receives them, indicating that synapses have the ability to transmit toxic tau proteins from one part of the brain to another.

In the opinion of Sílvia Pujals, a Ramón y Cajal researcher at the IQAC-CSIC, “this study demonstrates how superresolution microscopy, capable of visualizing structures at the nanoscale, has much potential in the study of molecular mechanisms implicated in diseases.

promising strategy

These data reinforce the hypothesis that stop the spread of the toxic form of tau protein at synapses can be a promising strategy to treat Alzheimer’s in the future, explains Lleó. “If we manage to block the passage of one neuron to another of the most pathological form of the tau protein, which are oligomers, surely we could stop the progression of the Alzheimer disease. Because we know that the disease progression It has to do with the expansion of the protein by the brain Explain.

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The principal investigator, Professor Tara Spires Jones of the UK Dementia Research Institute at the University of Edinburgh, notes that “we have known for over 30 years that tangles spread through the brain during Alzheimer disease, but how they spread remained a mystery. The protein deposits precede the death of neurons, contributing to the decreased cognitive ability. Stopping the spread of toxic Tau is a promising strategy to stop the disease in its tracks.”

Sonia Sirisi Dolcet, postdoctoral researcher in the Neurobiology of Dementias group at the IIB Sant Pau details that the Tau oligomers, which are the ones that travel through the synapse, “are a very early in the aggregation process of this protein. In other words, they are present in the very early stages of Alzheimer’s disease.” That is why, if they manage to develop Strategies to prevent the spread of this protein by the brain in these early stages, its progression could be prevented or halted.