Alzheimer's disease has been reversed in mice after experimenting scientists boosted the formation of new brain cells. A gene therapy fueled neurons in the hippocampus—a region vital for learning and remembering.
The study was published in the Journal of Experimental Medicine (JEM).
The breakthrough could lead to new treatments for the disease. The number of dementia cases worldwide is expected to triple to 150 million by 2050. There is no cure for the disease at present.
Lead author Professor Orly Lazarov, of the University of Illinois, Chicago, said: "Taken together, our results suggest augmenting neurogenesis may be of therapeutic value."
Experiments have shown the process is impaired in patients and mice with mutations linked to Alzheimer's, particularly in the hippocampus.
The U.S. team found increasing production of neurons rescued the lab rodent's defects. They were incorporated into memory circuits, restoring normal function. The study offers hope for a viable strategy. Current drugs target just the symptoms and not the cause.
Brain cells send electric signals. We keep making them throughout our lives. They are produced by neural stem cells. But the number of brain cells tail off as we age—and falls dramatically in people with Alzheimer's. Evidence appears to show that improving neurogenesis holds the key to treating dementia.
The hippocampus is the region of grey matter you need, for instance, to remember where you parked your car.
Prof. Lazarov said: "However, the role of newly formed neurons in memory formation, and whether defects in neurogenesis contribute to the cognitive impairments associated with Alzheimer's, is unclear."
In the study, stem cell survival was enhanced by deleting a gene called Bax, leading to the maturation of more neurons.
Afterward, the animals regained their spatial recognition and contextual memory skills. The tests included finding their way around a maze. Scans of healthy mice showed the circuits involved in storing memories include many newly formed neurons alongside older ones.
Neurons were fluorescently labeled, lighting up as they were activated during acquisition and retrieval. The memory-stowing loops of mice with Alzheimer's contained fewer neurons. But the integration of newly formed brain cells was restored when neurogenesis was increased.
Further analyses revealed there was also a rise in the number of tiny protrusions called dendritic spines. They connect neurons and are critical for memory formation.
When the researchers specifically inactivated the new neurons, mice with dementia lost any improvement in memory, confirming the results.
Prof. Lazarov added: "Our study is the first to show impairments in hippocampal neurogenesis play a role in the memory deficits associated with Alzheimer's by decreasing the availability of immature neurons for memory formation."
Alzheimer's and other forms of dementia affect more than 920,000 people in the U.K.—a figure that will reach a million within three decades.
Produced in association with SWNS.
This story was provided to Newsweek by Zenger News.
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