Researchers have identified a new Alzheimer’s target and created an experimental compound that blocks a damaging process inside brain cells. In mice, the treatment slowed nerve cell loss, reduced Alzheimer’s-related changes, and even appeared to promote healthier aging.
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Slowing the progression of Alzheimer’s disease is the goal of most existing treatments, but reversing it is much harder. That’s because once neurons are lost, the adult brain lacks the ability to replace them.
But new research, led by scientists at the University of South Carolina, has shown promise in regrowing neurons in brain organoids, and restoring cognition in mouse models of Alzheimer’s.
“After just two injections, these mice became smarter,” says Peisheng Xu, professor of pharmaceutics at the University of South Carolina and corresponding author of the new study, published in the journal Cell Biomaterials.
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The gold standard for studying movement within neurological networks involves injecting tracer substances into cerebrospinal fluid, the liquid surrounding the brain and spinal cord. But due to the extra volume introduced to the brain system, extra fluid can disrupt normal brain processes and often produces only a broad picture of fluid flow rather than highlighting pathways that could be linked to neurological disease.
“These injected tracers disturb the very system we’re attempting to measure,” said Yang. “We wanted to find a better way.”
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Scientists have long known that genetics play a role in Alzheimer’s disease risk. Some genetic markers appear to increase the likelihood of developing the condition, while others seem to offer a degree of protection against cognitive decline and brain aging.
One of the most important genes researchers study is called APOE. Everyone inherits two copies, but the specific version you carry may influence how resilient your brain is over time. In particular, one version called APOE4 is strongly linked to a higher risk of Alzheimer’s disease, while another, APOE2, is associated with lower risk and even exceptional longevity.
Now, new research may help explain why (and why some may be more resilient to aging than others).
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Scientists have identified new ways lithium chloride may interact with Alzheimer’s disease mechanisms at the cellular level.
A new study from the University of Eastern Finland (UEF) suggests lithium chloride may influence several cellular processes linked to Alzheimer’s disease.
Alzheimer’s disease (AD) is the most common type of dementia. One of its key features is the abnormal phosphorylation and buildup of Tau proteins inside brain cells, along with the accumulation of β-amyloid (Aβ) plaques.
Researchers have previously used lithium salts, especially lithium chloride and lithium carbonate, in cell and animal models of AD to reduce Tau hyperphosphorylation and aggregation. However, human clinical trials have produced inconsistent results, with some studies showing little or no improvement in cognitive function.
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A new nanotechnology treatment reversed Alzheimer’s symptoms in mice by restoring the brain’s natural cleanup system. The specially engineered nanoparticles helped clear toxic amyloid proteins from the brain and repair the blood-brain barrier, which normally protects and regulates the brain’s environment. In one striking experiment, elderly mice treated with the therapy later behaved like healthy younger mice.
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