The Alzheimer disease It is an unstoppable epidemic that increases in prevalence as the population ages, since one in 10 people older than 65 years suffers from this type of dementia, which is estimated to affect 46 million people worldwide, according to data from the Pasqual Maragall Foundation. One of the main characteristics of this neurodegenerative disease is the pathological accumulation in the form of neurofibrillary tangles of tau protein. These abnormal deposits spread through the circuits of the brain and interfere with communication between brain cells, altering their functions.
Now, and for the first time, researchers from the Dementia Neurobiology group at the Hospital de la Santa Creu i Sant Pau Research Institute – IIB Sant Pau have observed in human brains how these harmful proteins that accumulate in Alzheimer’s patients spread through the brain through synapsesa process that has been described in the prestigious scientific journal Neuron.
Synapses are the connection points between brain cells that allow chemical and electrical messages to circulate, a key process for normal brain function. Alzheimer’s disease causes the loss of these connections, which is an important predictor of Loss of memory and other intellectual functions in those affected.
If strategies can be developed to prevent the spread of the TAU protein in the brain in the early stages of Alzheimer’s, it could prevent or stop its progression
The research has been directed by the team of Professor Tara Spires-Jonesfrom 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 Institute for Advanced Chemistry of Catalonia (IQAC) of the Higher Council for Scientific Research (CSIC), and their findings provide new evidence that could be the key to slow the progress of Alzheimer’s. The study has been carried out within the framework of the European project COEN, financed by CIBERNED and coordinated by the Alberto Leónresearcher of the Neurobiology of Dementias group at IIB Sant Pau.
A key finding to slow the progression of Alzheimer’s
The researchers examined more than a million synapses from 42 people using novel techniques performed with high-power, super-resolution microscopes in collaboration with the IQAC-CSIC, which allowed visualization of protein flow within individual synapses. The researchers observed that small deposits of the Tau protein, known as oligomers, were on both sides of the synapses in people who died of Alzheimer’s. That is, both in the neuron that sends signals and in 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 the Silvia PujalsRamón y Cajal researcher at IQAC-CSIC, “this study demonstrates how super-resolution microscopy, capable of visualizing nanoscale structures, has great potential in the study of the molecular mechanisms involved in diseases.”
The findings support the hypothesis that stopping the spread of the toxic form of the Tau protein in synapses may be a promising strategy to treat Alzheimer’s disease in the future, explains Lleó. “If we manage to block the passage from one neuron to another of the most pathological form of the Tau protein, which are the oligomers, we could surely stop the progression of Alzheimer’s disease. Because we know that the progression of the disease has to do with the expansion of the protein in the brain.”
Tara-Spires Jones notes that “we have known for more than 30 years that tangles spread through the brain during Alzheimer’s disease, but how they spread remained a mystery. 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.”
Sònia 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 form in the aggregation process of this protein. That is, they are present in very early stages of Alzheimer’s disease. For this reason, if strategies can be developed to prevent the spread of this protein throughout the brain at these early stages, it could prevent or stop its progression.
Fuente: Higher Council for Scientific Research (CSIC)