Health

Alzheimer’s Stem Cell Therapy Study

A study by the University of California at San Diego (USA) showed that hematopoietic stem cell transplantation may protect against memory loss, neuroinflammation, and amyloid-B accumulation in mice with Alzheimer’s disease.

stem cell therapy they are already being used to treat various types of cancer and diseases of the blood and immune system. This new study, published in a scientific journal Cell reportstransplantation of hematopoietic stem cells and progenitor cells. effective in reversing multiple signs and symptoms of Alzheimer’s disease in a mouse model of the disease.

Mice injected with healthy hematopoietic stem cells showed preserved memory and cognition, reduced neuroinflammation, and significantly less accumulation of amyloid-B compared to other mice with Alzheimer’s disease.

Alzheimer’s disease is a very complex disease.therefore, any potential treatment should be aimed at multiple biological pathways. Our work demonstrates that transplantation of hematopoietic stem cells and progenitor cells can prevent complications of Alzheimer’s disease and may be promising therapeutic route for this disease“said the study’s lead author, Stephanie Cherki.

The success of therapy lies in its effect on microglia, a type of immune cell in the brain. Microglia are involved in various ways in the initiation and progression of Alzheimer’s disease. It is known that persistent inflammation of microglia may contribute to the development of Alzheimer’s disease, since the release of inflammatory cytokines, chemokines, and complement proteins leads to an increase in B-amyloid production.

Under healthy conditions, microglia also play an important role in removal of B-amyloid plaquesbut this function is impaired in Alzheimer’s disease. The subsequent accumulation of B-amyloid also puts pressure on other brain cells, such as endothelial cells, which affect blood flow to the brain.

Generate new microglia

The researchers wanted to see stem cell transplant can generate new, healthy microglia to slow the progression of Alzheimer’s disease. This group of scientists has already had success with similar stem cell transplants to treat mouse models. cystinosislysosomal storage disease and Friedreich’s ataxianeurodegenerative disease.

They performed systemic transplantation of healthy hematopoietic stem cells and wild-type progenitor cells into mice with Alzheimer’s disease and found that the transplanted cells differentiated into microglial-like brain cells.

They then evaluated the behavior of the animals and found that memory loss and neurocognitive decline were completely avoided in mice undergoing stem cell transplantation. These mice showed better object recognition and risk perception as well as normal levels of restlessness and movementcompared to untreated mice with Alzheimer’s disease.

By closely examining the brains of the animals, the researchers found that in mice given healthy stem cells, significant reduction in B-amyloid plaques in the hippocampus and cerebral cortex. The transplant also reduced microgliosis and neuroinflammation and helped maintain the integrity of the blood-brain barrier.

Finally, the researchers used transcriptome analysis to measure the expression of various genes in treated and untreated mice with Alzheimer’s disease. Those who have received stem cell therapy less cortical expression of genes associated with diseased microglia and less expression of genes in the hippocampus associated with diseased endothelial cells.

Combined transplantation of healthy hematopoietic stem cells and progenitor cells improved microglia healthwhich in turn protected from multiple levels of Alzheimer’s pathology.

A third group of mice injected with stem cells isolated from Alzheimer’s mice showed no signs of improvement, demonstrating that these cells stored information related to Alzheimer’s disease.

Future research will continue to explore how transplanted healthy cells bring about such dramatic improvements, and whether similar transplant strategies could be used to alleviate the symptoms of Alzheimer’s disease in humans.

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