With more than 5 million Americans living with Alzheimer's disease, the race is on to develop new treatments for the condition. Now, researchers from the Gladstone Institutes in San Francisco, CA, and the University of California-San Francisco reveal they have successfully reversed learning and memory deficits in mouse models of Alzheimer's through transplantation of healthy brain cells.
The research team, including senior author Dr. Yadong Huang, an associate investigator at the Gladstone Institutes and associate professor of neurology and pathology at UCSF, recently published their findings in the Journal of Neuroscience.
Alzheimer's disease is the most common form of dementia, characterized by memory, thinking and behavioral problems. Although the exact cause of Alzheimer's is unclear, past research has indicated that those who possess a gene called apolipoprotein E4 (apoE4) are at increased risk for the condition.
According to the researchers, the apoE4 gene - which is involved in 60-75% of Alzheimer's cases - causes a decline in inhibitory regulator cells that are crucial for normal brain activity.
They note that in particular, the gene is responsible for a decline of such cells in the hippocampus - a brain region responsible for memory - which is believed to contribute to learning and memory deficits typical of Alzheimer's disease.
For their study, Dr. Huang and colleagues wanted to test whether replenishing healthy inhibitory regulator cells in the brain could reverse learning and memory loss caused by the apoE4 gene.
Restoration of memory and learning function in mouse models 'very exciting'
The team transplanted inhibitory neuron progenitors - early-stage brain cells that can change into mature inhibitory regulator cells - into the hippocampus of two mouse models of Alzheimer's disease. One mouse model possessed the apoE4 gene, while the other had the apoE4 gene alongside a build-up of amyloid-beta - a protein also believed to play a role in Alzheimer's development.
The researchers found that the transplanted healthy inhibitory regulator cells not only survived in the hippocampus of both mouse models, but also successfully boosted inhibitory signaling and restored learning and memory function.
Furthermore, the team found that when they transplanted healthy inhibitory regulator cells into mice with both the apoE4 gene and an amyloid-beta build-up, the new cells also restored learning and memory deficits caused by amyloid-beta accumulation.
But the team notes that the new healthy cells did not influence amyloid-beta levels, indicating that cognitive restoration was not down to a reduction in amyloid-beta, nor did the protein interfere with the function of the transplanted cells.
Commenting on the team's findings, Dr. Huang says:
"This is a very important proof-of-concept study. The fact that we see a functional integration of these cells into the hippocampal circuitry and a complete rescue of learning and memory deficits in an aged model of Alzheimer's disease is very exciting.
This study tells us that if there is any way we can enhance inhibitory neuron function in the hippocampus, like through the development of small molecule compounds, it may be beneficial for Alzheimer disease patients."
Medical News Today has recently reported on an array of studies detailing potential ways to prevent Alzheimer's and improve diagnosis. Research presented at the Alzheimer's Association International Conference 2014 in Copenhagen, Denmark, revealed that eye and smell tests could offer early diagnosis of the condition, while other research suggests that a third of Alzheimer's cases may be preventable by changing lifestyle factors, such as giving up smoking and increasing physical activity.