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Harvard University: The Near Future of Cybernetics Transpires

Researchers are blurring the distinction between brain and machine, designing nanoelectronics that look, interact, and feel like real neurons. Camouflaged in the brain, this neurotechnology could offer a better way to treat neurodenerative diseases or control prosthetics, interface with computers or even enhance cognitive abilities.

Electrodes implanted in the brain help alleviate symptoms like the intrusive tremors associated with Parkinson’s disease but current probes face limitations due to their size and inflexibility. In a recent paper titled “Precision Electronic Medicine,” published in Nature Biotechnology, Shaun Patel, a faculty member at the Harvard Medical School and Massachusetts General Hospital, and Charles M. Lieber, the Joshua and Beth Friedman University Professor, argue that neurotechnology is on the cusp of a major renaissance. Throughout history, scientists have blurred discipline lines to tackle problems larger than their individual fields.

“The next frontier is really the merging of human cognition with machines,” says Patel. “Everything manifests in the brain fundamentally. All your thoughts, your perceptions, any type of disease.” He and Lieber see mesh electronics as the foundation for these machines, a way to design personalized electronic treatment for just about anything related to the brain. “Today, research focused at the interface between the nervous system and electronics is not only leading to advances in fundamental neuroscience, but also unlocking the potential of implants capable of cellular-level therapeutic targeting,” write the authors in their paper.

Geneticists Are Untangling the Mystery of Left-Handedness

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.

Brain, Liver and Muscle Rejuvenated

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].

Blue Brain finds how neurons in the mouse neocortex form billions of synaptic connections

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 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.

Removing Dysfunctional Microglia Prevents Amyloid-β Plaques

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.

Common Protein Fights Alzheimer’s Disease

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.