A groundbreaking study has revealed that hereditary Alzheimer’s disease can be transmitted via bone marrow transplants. This discovery challenges the traditional understanding of Alzheimer’s as a brain-centric condition and suggests a more systemic nature of the disease.
Key Takeaways
- Systemic Nature of Alzheimer’s: The study provides evidence that Alzheimer’s disease can be considered systemic, with amyloids outside the brain contributing to its development.
- Impact of Bone Marrow Transplants: Bone marrow stem cells from mice with a hereditary form of Alzheimer’s transferred the disease to healthy mice, accelerating its onset.
- Implications for Transplants and Transfusions: The findings advocate for the screening of blood, organ, and stem cell donors for Alzheimer’s disease to avoid its potential transmission.
The Study
Researchers from the University of British Columbia conducted a study where they transplanted bone marrow stem cells from mice carrying a hereditary version of Alzheimer’s disease into normal lab mice. The recipients developed Alzheimer’s disease at an accelerated rate, demonstrating that amyloid proteins from peripheral sources can induce Alzheimer’s in the central nervous system.
Systemic Implications
The study highlights the role of amyloid that originates outside of the brain in the development of Alzheimer’s disease. This shifts the paradigm of Alzheimer’s from being a disease that is exclusively produced in the brain to a more systemic disease. The researchers suggest that donors of blood, tissue, organ, and stem cells should be screened for Alzheimer’s disease to prevent its inadvertent transfer during blood product transfusions and cellular therapies.
Experimental Details
To test whether a peripheral source of amyloid could contribute to the development of Alzheimer’s in the brain, the researchers transplanted bone marrow containing stem cells from mice carrying a familial version of the disease—a variant of the human amyloid precursor protein (APP) gene. They performed transplants into two different strains of recipient mice: APP-knockout mice that lacked an APP gene altogether, and mice that carried a normal APP gene.
In this model of heritable Alzheimer’s disease, mice usually begin developing plaques at 9 to 10 months of age, and behavioral signs of cognitive decline begin to appear at 11 to 12 months of age. Surprisingly, the transplant recipients began showing symptoms of cognitive decline much earlier—at 6 months post-transplant for the APP-knockout mice and at 9 months for the “normal” mice.
Future Research
The researchers plan to test whether transplanting tissues from normal mice to mice with familial Alzheimer’s could mitigate the disease. They also aim to investigate whether the disease is transferable via other types of transplants or transfusions and to expand the investigation of the transfer of disease between species.
Funding and Support
This research was supported by the Canadian Institutes of Health Research, the W. Garfield Weston Foundation/Weston Brain Institute, the Centre for Blood Research, the University of British Columbia, the Austrian Academy of Science, and the Sullivan Urology Foundation at Vancouver General Hospital.
