A protein tied to ALS and dementia may have a much bigger role in disease than scientists realized. Researchers found that TDP43 controls a key DNA repair process, but when the protein becomes imbalanced, the repair system can spiral out of control, harming neurons and destabilizing DNA. The team also discovered that high levels of the protein are linked to increased mutation rates in cancer. The discovery places TDP43 at the center of both neurodegeneration and cancer biology.

A protein tied to ALS and dementia may have a much bigger role in disease than scientists realized. Researchers found that TDP43 controls a key DNA repair process, but when the protein becomes imbalanced, the repair system can spiral out of control, harming neurons and destabilizing DNA. The team also discovered that high levels of the protein are linked to increased mutation rates in cancer. The discovery places TDP43 at the center of both neurodegeneration and cancer biology.

Cocaine addiction isn’t simply a failure of willpower — it’s the result of lasting biological changes in the brain. Researchers at Michigan State University discovered that repeated cocaine use rewires communication between the brain’s reward system and the hippocampus, the region responsible for memory. A protein called DeltaFosB builds up with continued drug use and acts like a genetic switch, altering how neurons function and strengthening the brain’s drive to seek cocaine.

Cocaine addiction isn’t simply a failure of willpower — it’s the result of lasting biological changes in the brain. Researchers at Michigan State University discovered that repeated cocaine use rewires communication between the brain’s reward system and the hippocampus, the region responsible for memory. A protein called DeltaFosB builds up with continued drug use and acts like a genetic switch, altering how neurons function and strengthening the brain’s drive to seek cocaine.

Scientists have uncovered a crucial weakness in the malaria parasite that could open the door to new treatments. Researchers identified a protein called Aurora-related kinase 1 (ARK1) that acts like a traffic controller during the parasite’s unusual cell division process, ensuring its genetic material is properly separated as it multiplies. When scientists switched off ARK1 in laboratory experiments, the parasite could no longer replicate correctly and failed to complete its life cycle in both humans and mosquitoes—effectively halting its ability to spread.

Scientists have uncovered a crucial weakness in the malaria parasite that could open the door to new treatments. Researchers identified a protein called Aurora-related kinase 1 (ARK1) that acts like a traffic controller during the parasite’s unusual cell division process, ensuring its genetic material is properly separated as it multiplies. When scientists switched off ARK1 in laboratory experiments, the parasite could no longer replicate correctly and failed to complete its life cycle in both humans and mosquitoes—effectively halting its ability to spread.