As we age, changes occur throughout our body. Certain parts of the brain shrink, especially those important for learning and other complex activities. In other regions, communication between neurons can be reduced, as can blood flow. The brain generally shrinks to some degree in healthy aging, but, surprisingly, it does not lose neurons in large quantities. However, in Alzheimer’s disease, the damage is widespread, as many neurons stop working, lose connections with other neurons and die. Alzheimer’s disrupts vital processes for neurons and their networks, including communication, metabolism and repair.
Is there any solution to this process? A recent study, conducted by experts from the Molecular Biology “Severo Ochoa” (CBMSO, CSIC-UAM) and published in the Journal of Neuroscience, suggests yes.
Dysfunctional neurons in the hippocampus of adult female mice modified to manifest dementia can be repaired and reconnected to distant parts of the brain according to the results. The similarity between the mouse model and the human condition underscores the therapeutic potential of attacking these cells in patients with dementia.
Compared to the control subjects, the researchers, led by María Llorens-Martín, observed surprisingly similar alterations in newborn neurons of their mouse model and human brain tissue of patients with frontotemporal dementia. In mice, the chemical activation of cells and the placement of animals in a stimulating environment with wheels and toys reversed the alterations and restored part of the connectivity interrupted by dementia. If translated into humans, these results suggest potentially new directions to combat cognitive impairment in the elderly.
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