Lifeboat Foundation

Circa 2013

One of the greatest aspirations of the human mind has been to realize machines that surpass its cognitive intelligence. The rapid expansion in computing power, about to exceed the equivalent of the human brain, has yet to produce such a machine. The article by Neftci et al. in PNAS (1) offers a refreshing and humbling reminder that the brain’s cognition does not arise from exacting digital precision in high-performance computing, but rather emerges from an extremely efficient and resilient collective form of computation extending over very large ensembles of sluggish, imprecise, and unreliable analog components. This observation, first made by John von Neumann in his final opus (2), continues to challenge scientists and engineers several decades later in figuring and reproducing the mechanisms underlying brain-like forms of cognitive computing.

Related developments are currently unfolding in collaborative initiatives engaging scientists and engineers, on a grander scale, in advancing neuroscience toward understanding the brain. In parallel with the Human Brain Project in Europe, the Brain Research through Advancing Innovative Neurotechnologies Initiative promises groundbreaking advances in enabling tools for revolutionizing neuroscience by developing nanotechnology to probe brain function at greatly increased spatial and temporal detail. Engineers are poised to contribute even further in revolutionizing such developments in neuroscience. In this regard it is helpful to relate the inquisitive nature of science—analysis—to the constructive power of engineering, synthesis.

Circa 2012

M.I.T. scientist Sebastian Seung describes the audacious plan to find the connectome—a map of every single neuron in the brain. Here, he says, is the secret of human identity.

The research team, led by Todd Lencz, PhD, with Itsik Pe’er, PhD, Tom Maniatis, PhD, and Erin Flaherty, PhD, of Columbia University, carried out a genetic study identifying a single letter change in the DNA code in the PCDHA3 gene that is associated with schizophrenia. The affected gene makes a type of protein called a protocadherin, which generates a cell surface “barcode” required for neurons to recognize, and communicate with, other neurons. They found that the PCDHA3 variant blocks this normal protocadherin function.

The discovery was made possible by the special genetic characteristics of the samples studied by Lencz’s team—patients with schizophrenia and healthy volunteers drawn from the Ashkenazi Jewish population. The Ashkenazi Jewish population represents an important population for study based on its unique history. Just a few hundred individuals who migrated to Eastern Europe less than 1000 years ago are the ancestors of nearly 10 million Ashkenazi Jews today. This lineage, combined with a tradition of marriage within the community, has resulted in a more uniform genetic background in which to identify disease-related variants.

“In addition to our primary findings regarding PCDHA3 and related genes, we were able— due to the unique characteristics of the Ashkenazi population—to replicate several prior findings in schizophrenia despite relatively small sample sizes,” said Lencz, professor in the Institute of Behavioral Science at the Feinstein Institutes. “In our study, we demonstrated this population represents a smart, cost-effective strategy for identifying disease-related genes. Our findings allow us to zero in on a novel aspect of brain development and function in our quest to develop new treatments for schizophrenia.”

It is well established that rare, damaging genetic variants with strong effects contribute to autism. Although individually rare, these variants are collectively common: Clinical genetic testing identifies them in at least 25 percent of autistic people. Studies of these variants have implicated more than 100 genes — and counting — in autism.

Identifying these genes is important — not only for clinical care, but also for advancing our understanding of the neural circuits and processes involved in autism or in its core traits. It creates the opportunity to develop therapies targeted to specific molecular diagnoses. And as we learn more about these genes and the consequences of variants that disrupt their function, we have the potential to better understand the mechanisms underlying cases of autism in which a definitive genetic diagnosis cannot yet be made.

But the genetic findings in people with autism are not unique; deleterious variants in the same genes are also implicated in other neurodevelopmental conditions, such as intellectual disability, epilepsy, attention deficit hyperactivity disorder and schizophrenia. Specific genes and variants do not map neatly onto categorical clinical diagnoses or the core cognitive and behavioral traits that define them. In fact, there is not yet a single example of a gene that, when mutated, increases the likelihood of autism but not of other neurodevelopmental conditions.

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The Artemis program is supposed to usher in a new age of lunar mining, especially for water ice. But how, exactly?

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This progressive trance set is labeled SYNTELLECTUS and is inspired by The Syntellect Hypothesis, a recent best-selling book of mine… If you remember, SYNTELLECTUS refers to a neologism Holo Syntellectus — a new hybrid species emerging as a syntellect, [phase-transitioning to] one global mind… Enjoy!

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New York approves a power cable for Deepwater Wind South Fork; Give Solar works with Habitat for Humanity to provide solar for homeowners.

Fan speeds clock in over 11000 RPM.

Dynatron rolls out the A38, a robust CPU air cooler for AMD Ryzen Threadripper and EPYC processors.