Health & Medicine, UK (Commonwealth Union) – Dementia is a devastating condition that affects millions of people across the globe, causing a progressive decline in cognitive abilities and memory. While the exact causes of dementia are not officially established, researchers have made significant strides in unraveling the role of the tau protein in the development and progression of neurodegenerative disorders.
The tau protein, also known as microtubule-associated protein tau, is found predominantly in nerve cells (neurons) and plays a crucial role in stabilizing and maintaining the structure of microtubules, which are essential for proper cell functioning and transport of nutrients within neurons. In healthy neurons, tau protein helps support the intricate network of microtubules, allowing them to function effectively.
However, in certain neurodegenerative disorders, such as Alzheimer’s disease, frontotemporal dementia, and other tauopathies, the tau protein undergoes abnormal modifications and accumulates in the brain, forming tangles or aggregates. These tau tangles disrupt the normal functioning of neurons and contribute to their degeneration and eventual death, leading to the cognitive decline observed in dementia patients.
New details in regards to the spread of the tau proteins that gather up in the brains of individuals with Alzheimer’s disease could be the key to halting the progression of the condition, according to recent research.
Scientists have found that synapses, transmitting essential signals via the brain, transport toxic tau protein around the brain as well.
Bigger clumps of tau referred to as tangles are produced in brain cells and are one of the properties that define Alzheimer’s disease. As these tangles move across the brain when the disease occurs, the brain function is lowered.
The research was led by the University of Edinburgh, which draws its attention to synapses, connections that permit the flowing of chemical as well as electrical messages between brain cells which are significant for healthy brain function. Alzheimer’s disease targets synapse where the loss of them heavily forecasts lower memory along with thinking abilities.
The research had; scientists evaluate over a million synapses from 42 individuals applying powerful microscopy methods to visualize proteins inside individual synapses.
Researchers noted that small clumps of tau, referred to as tau oligomers can be seen within the synapses of individuals that died from Alzheimer’s disease.
The tangles of tau oligomers had been noticed at both ends of the synapse. This included the brain cell transmitting signals and the brain cell getting signals.
Researchers had noted in studies that the oligomers hopped from one side of the synapse to the other, spreading the tau via the brain.
Bringing down oligomeric tau at synapses could be a positive strategy to halt the disease progression in the years ahead according to the experts.
Alzheimer’s disease is the most common form of dementia, with roughly 900,000 individuals right now with the disease across the UK. This number is set to increase to almost 1.6 million in 2040, as indicated by researchers.
The findings appeared in the journal Neuron. The study team consisted of researchers from the University of Edinburgh, the UK Dementia Research Institute, the Institut d’Investigacions Biomèdiques Hospital de Sant Pau along with the Institute for Advanced Chemistry of Catalonia (Barcelona).
“We have known for over 30 years that tangles spread through the brain during Alzheimer’s disease, but how they spread has remained a mystery. Wherever tangles appear in the brain, neuron death follows, contributing to the decline in cognitive ability. Stopping the spread of toxic tau is a promising strategy to stop the disease in its tracks,” said Professor Tara-Spires Jones who led the research from the UK Dementia Research Institute at the University of Edinburgh. The study is likely to play a key contribution to the growing number of studies on tau protein over the years.
