A new Yale study has found a promising target for treating the brain fog that can follow COVID-19 and offers new insight into a hypothesis about the origin of Alzheimer’s disease.

One of the hallmarks of Alzheimer’s disease is the presence of plaque formed by the buildup of amyloid beta peptides (short chains of amino acids) in and around brain cells. Some researchers suspect that amyloid beta, which is structurally similar to antimicrobial peptides, protects the brain against bacteria, viruses, parasites, and fungal infections. Because the blood-brain barrier tends to lose its integrity in Alzheimer’s disease patients, the accumulation of amyloid beta might be a signal that pathogens are infiltrating the brain.

In a new study published in Science Advances, Yale researchers investigated whether infection by SARS-CoV-2—the virus that causes COVID-19—can trigger Alzheimer’s disease-like amyloid beta buildup, leading to neurological impairments like brain fog.

Scientists grew 400+ brain cell types in the lab—an unprecedented step toward curing neurological diseases.

Significant brain defects known as Chiari malformations could be down the genes some of us have inherited from Neanderthals, according to a new study, causing a mismatch between brain shape and skull shape.

The study focuses on Chiari malformation type I (CM-I), where the lower part of the brain extends too far into the spinal cord – typically linked to having a smaller-than-normal occipital bone at the back of the skull. It can lead to headaches, neck pain, and more serious conditions, and is thought to affect up to 1 in 100 people.

Several other ancient human species had different skull shapes to our own, and a previous study published in 2013 put forward the idea that interbreeding between Homo sapiens and these other hominins may be a root cause of Chiari malformation type I (CM-I), the mildest type of the group.