Khaberni - French researchers have made significant scientific progress in understanding Alzheimer's disease, following the discovery of the role of a specific type of brain cells in the progression of the disease.
A recent study conducted by researchers from the French National Institute of Health and Medical Research, University of Lille, and the University Hospital in Lille suggests that dysfunction of these cells may be one of the main reasons for the accumulation of tau protein in the brain, which is one of the prominent biological markers associated with the disease, according to the official website of the French National Institute of Health.
Alzheimer's is one of the most prevalent neurodegenerative diseases in the world, characterized by gradual impairments in memory and cognitive abilities such as decision-making, thinking, and temporal and spatial orientation.
The disease occurs as a result of gradual deterioration of the nerve cells in the hippocampus, responsible for memory, before gradually spreading to other parts of the brain.
One of the main biological markers of the disease is the abnormal accumulation of tau protein within the nerve cells, a protein that plays an important role in maintaining the stability of the internal structure of the nerve cells.
What happens to "tau" protein in normal condition?
In a healthy brain, nerve cells produce "tau" protein in limited amounts, and it is secreted into the cerebrospinal fluid (the fluid surrounding the brain and spinal cord). Afterwards, it is gradually eliminated by transferring into the bloodstream.
However, in individuals with Alzheimer's disease, the structure of this protein changes, becoming unable to perform its normal function, and it begins to accumulate inside the nerve cells pathologically.
Over time, this accumulation leads to the disruption of the nerve cells' function, then their death, causing cognitive decline and memory loss.
The new study focused on a type of brain cells called "Tanycytes," which are located in an area near the brain ventricles, and play a role in regulating the exchange between blood and cerebrospinal fluid.
The research team, led by scientist Vincent Prevot, has studied these cells for over twenty years, revealing that they are responsible for the transport of some important hormones, such as leptin, which controls appetite and energy balance in the body.
However, the new study revealed for the first time that these cells have a direct role in the transport of Tau protein from the brain to the blood.
How did the scientists make this discovery?
The researchers relied on a series of precise experiments. Initially, they injected Tau protein into the cerebrospinal fluid of animal models, then tracked its path using fluorescence imaging techniques.
The results showed that tanycytic cells capture Tau protein from the cerebrospinal fluid and then transport it through their cellular extensions until it reaches the blood capillaries, where it is disposed of into the bloodstream.
Based on these results, the researchers hypothesized that these cells form the main pathway for the removal of "tau" protein from the brain.
To test this hypothesis, the researchers disrupted the function of tanycytic cells using genetic modification that allows for the production of botulinum toxin inside these cells, preventing them from performing their function.
The results showed that disrupting these cells led to the cessation of the transfer of Tau protein from the cerebrospinal fluid to the blood, causing its accumulation inside the brain.
The scientists also observed that mice with disabled tanycytic cells displayed early symptoms of dementia compared to others.
To confirm the validity of these results, the researchers also studied the brains of people who died from Alzheimer’s disease.
Analyses revealed the presence of Tau protein inside the tanycytic cells of the patients, and the scientists observed that these cells were clearly damaged.
Their cellular extensions were fragmented and severed, which disrupted the natural pathway that allows for the transfer of the protein from the cerebrospinal fluid to the blood.
Interestingly, this damage was not observed in the brains of patients suffering from other types of dementia, indicating that it might be specific to Alzheimer's disease.
The researchers believe that this discovery may open new avenues for developing treatments for Alzheimer's disease, as if the health of the tanycytic cells plays a crucial role in preventing the accumulation of "tau" protein, these cells may become a new therapeutic target.
