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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].

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.

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.

One way that scientists can non-invasively study the human brain is by growing “mini-brains,” clusters of brain cells each about the size of a pea, in the lab. In a fascinating progression of this line of research, a team this week reports that they observed human-like brainwaves from these organoids.

Previous studies of mini-brains have demonstrated movement and nerve tract development, but the new study from researchers at the University of California San Diego, led by biologist Alysson Muotri, is the first to record human-like neural activity. In their paper, published in Cell Stem Cell on Thursday, the researchers write that they observed brain wave patterns resembling those of a developing human. This sophistication in the in vitro model is a step to enable scientists to use mini-brains to study brain development, model diseases, and learn about the evolution of brains, according to Muotri.

https://www.youtube.com/watch?v=pVW9UNQVRtk