The human brain builds mental representations of the world based on the signals and information detected via the human senses. While we perceive simultaneously occurring sensory stimuli as being synchronized, the generation and transmission speeds of individual sensory signals can vary greatly.

Researchers at the Institute of Molecular and Clinical Ophthalmology Basel (IOB), University of Basel and Eidgenossische Technische Hochschule (ETH) Zurich recently carried out a study aimed at better understanding how the human visual system achieves this synchronization, regardless of the speed at which visual signals travel. Their paper, published in Nature Neuroscience, reports a previously unknown mechanism through which the retina synchronizes the arrival times of different visual signals.

“We can see because photoreceptors in the retina at the back of our eyes detect light and encode information about the visual world in the form of electrical signals,” Felix Franke and Annalisa Bucci, senior author and first author of the paper, respectively, told Medical Xpress.

Parkinson’s disease (PD) involves toxic protein buildup and energy failure in neurons. Continuously breathing low-oxygen air protected mice from PD-like neuronal loss and reversed symptoms, even after they began, suggesting that hypoxia may protect neurons.

Researchers have suspected for some time that the link between our gut and brain plays a role in the onset of Parkinson’s disease.

A recent study identified gut microbes likely to be involved and linked them with decreased riboflavin (vitamin B2) and biotin (vitamin B7), suggesting an unexpectedly simple treatment that may help: B vitamins.

“Supplementation therapy targeting riboflavin and biotin holds promise as a potential therapeutic avenue for alleviating PD symptoms and slowing disease progression,” Nagoya University medical researcher Hiroshi Nishiwaki said when the study was published in May 2024.

Ever since Biogen and Eisai’s Aduhelm (aducanemab) was approved in 2021 as the first antibody to treat Alzheimer’s disease by clearing amyloid plaques from the brain, the modality has been dogged by a serious side effect: brain bleeding called amyloid-related imaging abnormalities, or ARIA.

Now, researchers from Denali Therapeutics have debuted an antibody that can cross the blood-brain barrier and attack amyloid, but without triggering this potentially life-threatening complication.