Lifeboat Foundation

A series of genetic variants can influence handedness, according to a new paper.

No, researchers have not discovered a “handedness gene.” But through brain imaging of 9,000 people in the United Kingdom, researchers devised a list of genetic variations that contribute to the way different brain processes end up on either side of the brain. This, in turn influences handedness—and can also influence whether someone will develop certain neurological diseases, according to the paper published in the journal Brain.

Age-related changes to the signals sent and received by our cells travelling via the bloodstream are one of the hallmarks of aging. A team of researchers, including Drs. Irina and Michael Conboy, has published the results of a new study suggesting that rejuvenation might be achieved by the calibration of these signals found in the blood [1].

The search for rejuvenation

The Conboys had done earlier research in joining of the circulatory systems between young and old animals, a process known as parabiosis, and they showed that tissue aging was not a one-way street and could be rapidly reversed in a matter of weeks, given access to the beneficial signaling from the younger animal [2].

Human rights law isn’t ready to protect your brain’s privacy in the neurotechnology era, says Marcello Ienca.

New research reveals how increasing brain stiffness as we age causes brain stem cell dysfunction, and demonstrates new ways to reverse older stem cells to a younger, healthier state.

States of mind that the legal system cares about — memory, responsibility and mental maturity — have long been difficult to describe objectively, but neuroscientists are starting to detect patterns. Coming soon to a courtroom near you?

Researchers at EPFL’s Blue Brain Project, a Swiss brain research Initiative, have combined two high profile, large-scale datasets to produce something completely new—a first draft model of the rules guiding neuron-to-neuron connectivity of a whole mouse neocortex. They generated statistical instances of the micro-connectome of 10 million neurons, a model spanning five orders of magnitude and containing 88 billion synaptic connections. A basis for the world’s largest-scale simulations of detailed neural circuits.

Identifying the connections across all neurons in every region of the neocortex

The structure of synaptic connections between neurons shapes their activity and function. Measuring a comprehensive snapshot of this so-called connectome has so far only been accomplished within tiny volumes, smaller than the head of a pin. For larger volumes, the long-range connectivity, formed by bundles of extremely thin but long fibers, has only been studied for small numbers of individual neurons, which is far from a complete picture. Alternatively, it has been studied at the macro-scale, a ‘zoomed-out’ view of average features that does not provide single-cell resolution.

The macrophages resident in the brain and spinal cord appear to be a key element in the progression of Alzheimer’s disease, according to the results of a new mouse study.

Microglial mayhem

As we age, our immune cells become increasingly dysfunctional; once-helpful cells can behave in harmful ways, promoting persistent inflammation, impairing tissue regeneration, and possibly also facilitating the progression of age-related diseases.

In a recent study, a team of researchers has discovered that a naturally occurring protein called Lipocalin-type prostaglandin D synthase (L-PGDS) prevents, and can destroy, the protein aggregates associated with Alzheimer’s disease.

Surprisingly common and with critical functions

L-PGDS is a common protein, second only to albumin, in the human brain. It provides several critical functions, including regulation of processes and protection against further damage from ischemic strokes. It has been shown to be a molecular chaperone, preventing amyloid beta from forming the deadly aggregates associated with Alzheimer’s, and, perhaps most importantly, it has been shown to destroy aggregates that already exist. Not surprisingly, people who suffer from Alzheimer’s disease lack adequate amounts of this critical protein.

C.A. Trujillo et al. Complex oscillatory waves emerging from cortical organoids model early human brain network development. Cell Stem Cell. Vol. 25, October 3, 2019, p. 1. doi: 10.1016/j.stem.2019.08.002.