In a new Science Translational Medicine study, Northwestern University scientists have pinpointed when and where toxic proteins accumulate within the brains of Alzheimer’s patients — and discovered a decades-old Food and Drug Administration (FDA)-approved drug that can stop the accumulation process before it even begins. Existing human clinical data also showed the drug slowed the progression of Alzheimer’s pathology.

By studying animal models, human neurons and brain tissue from high-risk patients, the team discovered a particularly toxic protein fragment, called amyloid-beta 42, accumulates inside neurons’ synaptic vesicles — the tiny packets that neurons use to send signals. But, when the scientists administered levetiracetam (an inexpensive, decades‑old anti‑seizure drug) to the animals and human neurons, the drug prevented neurons from forming amyloid-beta 42.

Brain cells are constantly swallowing material from the fluid that surrounds them — signaling molecules, nutrients, even pieces of their own surfaces — in a process known as endocytosis that is essential for learning, memory and basic neural upkeep.  

Now, new research by Penn State scientists has revealed this vital process may be governed by a previously unknown molecular gatekeeper: a lattice‑like structure just beneath the surface of brain cells, or neurons, called the membrane‑associated periodic skeleton or MPS.  

For years, scientists have worked to uncover how the brain responds to mechanical forces and electromagnetic waves. Computer models offer useful simulations, but they don’t fully capture what goes on inside a living brain. Now, the team from Mizzou’s College of Engineering is working to close that gap by developing 3D-printed models of an artificial human brain.