Neuron skeleton may offer new target to fight Alzheimer's

Penn State researchers have found that a lattice-like structure inside neurons acts as a gatekeeper controlling what cells absorb. When the structure weakens, neurons take in more harmful proteins linked to Alzheimer's disease. Stabilizing it could lead to new treatment strategies.

The membrane-associated periodic skeleton, or MPS, sits just beneath the surface of neurons. It regulates endocytosis, the process by which cells pull in material from their surroundings.

Experiments showed that disrupting the MPS caused neurons to absorb substances faster. This included amyloid precursor protein, which breaks down into a toxic fragment associated with Alzheimer's.

"We discovered that this membrane skeleton is actively regulating the nutrient uptake process of neurons," said Ruobo Zhou, the study's corresponding author. Lead author Jinyu Fei added that the findings could open doors for therapies aimed at preserving the structure.

The work, funded by the National Institutes of Health, was published in Science Advances. Researchers used super-resolution imaging on lab-grown neurons to track the effects.

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Microscopic illustration of neurons showing proteins helping misfolded alpha-synuclein enter brain cells in Parkinson's research
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Yale study identifies two neuron-surface proteins that help misfolded alpha-synuclein enter brain cells

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Researchers at Yale School of Medicine say they have identified two proteins on the surface of neurons that help shuttle misfolded alpha-synuclein—a key protein implicated in Parkinson’s disease—into healthy cells, a finding that could point to new strategies aimed at slowing progression.

Researchers have identified a previously unknown mechanism called karyoptosis that appears to drive the death of brain cells in Alzheimer's disease and frontotemporal dementia. The discovery, based on analysis of human brain tissue, points to a potential new target for treatments aimed at slowing neuron loss.

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Researchers from the Institute for Bioengineering of Catalonia and collaborating institutions report that engineered “supramolecular” nanoparticles restored aspects of blood-brain barrier function in Alzheimer’s-model mice, rapidly lowering brain amyloid-β and producing improvements on behavioral and memory tests.

Researchers at the Indiana University School of Medicine have identified the enzyme IDOL as a potential new target for treating Alzheimer's disease. Laboratory studies showed that removing the enzyme from neurons reduced amyloid plaques and improved brain cell communication.

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Researchers at Baylor College of Medicine report that tubulin—the building block of microtubules—can shift Tau and alpha-synuclein inside cellular condensates away from disease-linked aggregation and toward roles that support healthy neurons.

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