Beijing, April 1st (Zhang Mengran Reporting) - A study published in the latest issue of the journal "Stem Cell Reports" reveals that familial Alzheimer's disease can be transmitted through bone marrow transplantation. When researchers transplanted bone marrow stem cells from mice with genetic Alzheimer's disease into normal laboratory mice, the recipients developed Alzheimer's disease, and the progression of the disease was faster.
This study transforms Alzheimer's disease from a condition solely produced in the brain into a systemic disease. Researchers suggest that screening for Alzheimer's disease should be conducted on blood, tissues, organs, and stem cell donors to prevent inadvertent transmission during blood product transfusions and cell therapies.
Researchers transplanted bone marrow containing stem cells from mice with familial Alzheimer's disease. When amyloid precursor protein (APP) genes are cleaved, misfolded, and aggregated, amyloid plaques are formed, which are a hallmark of Alzheimer's disease. They transplanted into two different strains of recipient mice: APP gene knockout mice and mice carrying normal APP genes.
In this genetic model of Alzheimer's disease, mice typically begin to develop plaques at 9-10 months old, with signs of declining cognitive abilities appearing at 11-12 months old. Surprisingly, cognitive decline symptoms began in the transplanted recipients early: 6 months after transplantation for the APP knockout mice and 9 months after transplantation for the "normal" mice.
By further observing the disease transfer in mice, the team concluded that mutated genes in donor cells can cause disease, and animals carrying normal APP genes are susceptible to the disease. This suggests that the disease can be transmitted to healthy recipients.
Since transplanted stem cells are hematopoietic cells, meaning they can develop into blood and immune cells but not neurons, researchers demonstrated amyloid plaques in the brains of APP knockout mice, indicating that Alzheimer's disease may be caused by amyloid produced outside the central nervous system.
Furthermore, the source of the mouse disease is the human APP gene, indicating that mutated human genes can transfer the disease to different species.
