Some research has pointed to the loss of smell as one of the symptoms prior to neurodegenerative diseases such as Alzheimer’s. Now, an investigation carried out by members of the Frailty and Healthy Aging area of the CIBER (CIBERFES) and the University of Valencia (UV) have found the possible cause of this anosmia and other cognitive problems that occur in patients with Alzheimer’s
As explained in the publication of the journal Molecular Neurobiology, in Alzheimer’s the precursor cells of new neurons have an alteration in the cell cycle and an aging that could affect their ability to migrate. This neuronal migration is a process in which complex interactions take place that cause stem cells and neural progenitors to proliferate, differentiate and move to the appropriate position.
And it is that in the brain there are two areas where new neurons are formed and differentiate throughout life, and the main one is the subventricular zone of the forebrain, which is where the neuronal migration described above occurs. This study has focused on the process of formation of new neurons, which is altered in Alzheimer’s, reducing proliferation and neuronal creation, which leads to cognitive damage.
In search of a new approach to Alzheimer’s
The tests, done on mice, showed that those with Alzheimer’s had a deficit in cell migration in the subventricular neural niche, due to an aging state of the new neurons. This cellular senescence begins as a response to stress and damage to a cell, which causes it to have alterations in its ability to multiply.
Although new neurons are created, aging makes them unable to migrate, so they accumulate in the subventricular neural niche, promoting cognitive damage in Alzheimer’s
These cells that are aged paralyze their cell cycle, but they do not die, so they remain active and generate substances that are harmful to their environment, which accumulate in body tissues and are essential in the development of different pathologies, such as cancer. or Alzheimer’s. Therefore, new neurons are created, but aging makes them unable to migrate, remaining accumulated in the subventricular neural niche, which grows abnormally in the observed mice.
“In humans, this neurogenic disability has not been described yet, but it could be the explanation for the loss of smell suffered by Alzheimer’s patients from the very early stages of the disease, since the neurogenic niche of the subventricular zone is the one that provides new neurons to the olfactory bulb”, explains José Viña, member of CIBERFES at the University of Valencia and one of the main authors of the work.
The researchers have also shown that other kinds of brain cells are also created in this neural niche, which, if this same aging process and changes in migration occur, could also be the cause of other cognitive problems associated with Alzheimer’s disease. “The results of this work could contribute to a new approach to Alzheimer’s based on senolytic compounds or pro-neurogenic factors”, the authors conclude.
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