Lifeboat Foundation

Panpsychism is a disruptive theory put forward by some philosophers and neuroscientists. It proposes that human consciousness is only one of many forms of consciousness in…

A good night’s sleep can work wonders for both mind and body. But what is it that determines how much we need to sleep, and what can cause us to sleep more deeply?

In a new study, researchers from the University of Tsukuba have now provided some answers, revealing a signaling pathway within brain cells that regulates the length and depth of sleep.

“We examined genetic mutations in mice and how these affect their patterns of sleep,” says senior author of the study, Professor Hiromasa Funato. “We identified a mutation that led to the mice sleeping much longer and more deeply than usual.” The researchers found that this was caused by low levels of an enzyme called histone deacetylase 4 (HDAC4), which is known to suppress the expression of target genes.

Frankly I’m pretty stoked about getting my brain inside a computer and living forever.

Biotech startup Lucy Therapeutics is developing mitochondrial-based small molecule therapies for neurological diseases and recently revealed the first two drugs to emerge from its lead programme targeting Parkinson’s. The company, which takes its name from the 3.2-million-year-old fossil of an ancestor of humankind, presented “promising preclinical data” at the Michael J Fox Foundation’s Parkinson’s Disease Therapeutics Conference in October.

The data shown by Lucy Therapeutics demonstrated that its compounds were able to reverse mitochondrial dysfunctions linked to Parkinson’s. In cellular models of the disease, the drugs boosted levels of cellular energy molecule ATP, prevented the death of neurons, and reduced levels of other hallmarks of Parkinson’s, including a-synuclein.

Longevity. Technology: Mitochondria are widely known as the ‘power generators’ within our cells, and their dysfunction has been linked to a range of age-related diseases. But the role of mitochondria extends beyond cellular energy as they also dictate many of a cell’s key functions. Lucy Therapeutics was founded on the hypothesis that diseases with rate-limiting steps involving mitochondrial dysfunction can potentially be treated by modulating key mitochondrial protein targets. To find out more, we caught up with the company’s founder and CEO, Dr Amy Ripka.

Biological supramolecular assemblies, such as phospholipid bilayer membranes, have been used to demonstrate signal processing via short-term synaptic plasticity (STP) in the form of paired pulse facilitation and depression, emulating the brain’s efficiency and flexible cognitive capabilities. However, STP memory in lipid bilayers is volatile and cannot be stored or accessed over relevant periods of time, a key requirement for learning. Using droplet interface bilayers (DIBs) composed of lipids, water and hexadecane, and an electrical stimulation training protocol featuring repetitive sinusoidal voltage cycling, we show that DIBs displaying memcapacitive properties can also exhibit persistent synaptic plasticity in the form of long-term potentiation (LTP) associated with capacitive energy storage in the phospholipid bilayer. The time scales for the physical changes associated with the LTP range between minutes and hours, and are substantially longer than previous STP studies, where stored energy dissipated after only a few seconds. STP behavior is the result of reversible changes in bilayer area and thickness. On the other hand, LTP is the result of additional molecular and structural changes to the zwitterionic lipid headgroups and the dielectric properties of the lipid bilayer that result from the buildup of an increasingly asymmetric charge distribution at the bilayer interfaces.

Ablation of primary cilia in the striatum did not affect the object recognition memory, as evidenced by the more time mice spent with the novel object than the old object (Fig. 4e, f). Similarly, in the novel location recognition assay, IFT88-KO spent more time with the novel location than the old location (Fig. 4g, h), indicating a normal spatial memory. In addition, the contextual memory, measured using the fear conditioning test, was intact in the IFT88-KO mice, as revealed by the similar freezing time on the test day compared with the control mice (Fig. 4i).

The expression of the immediate-early gene cFos was used as a molecular marker of neural activity. We examined cFos immunoreactivity (number of cFos-positive cells) in structures that are parts of striatal circuits and those known to project to or receive projections from the striatum (Fig. 5a, b). First, the rostral dorsal striatum, but not the caudal striatum of IFT88-KO mice, exhibited a significant decrease of cFos immunoreactivity (Fig. 5c, d). Within the basal ganglia circuit, there was a trend for cFos immunoreactivity reductions in the output regions (SNr and the GPm), but not in the nuclei of the indirect pathway structures (lateral globus pallidus and subthalamic nucleus) (Fig. 5c, d). The main input regions to the striatum include the dopaminergic neurons of the substantia nigra pars compact (SNc) and the glutamatergic neurons of the cortices.

Perception generally feels effortless. If you hear a bird chirping and look out the window, it hardly feels like your brain has done anything at all when you recognize that chirping critter on your windowsill as a bird.

In fact, research in Psychological Science suggests that these kinds of audio cues can not only help us to recognize objects more quickly but can even alter our visual perception. That is, pair birdsong with a bird and we see a bird—but replace that birdsong with a squirrel’s chatter, and we’re not quite so sure what we’re looking at.

“Your brain spends a significant amount of energy to process the sensory information in the world and to give you that feeling of a full and seamless perception,” said lead author Jamal R. Williams (University of California, San Diego) in an interview. “One way that it does this is by making inferences about what sorts of information should be expected.”

Horgan: Okay, maybe I have been too critical. But can you tell readers, briefly, why they should take panpsychism seriously?

Mørch : Physicalism and dualism are the two main alternatives to panpsychism.

Physicalism implies that consciousness doesn’t exist. Physical science cannot capture what it’s like for someone to have conscious experiences, such as seeing red or being in pain, or any of the qualitative or subjective features of consciousness. So if consciousness is physical, it’s not qualitative or subjective, and therefore not really consciousness after all.

Year 2019 😗

Scientists have shown how a drug cocktail of four compounds can convert glia, or support cells, next to damaged neurons into new working neurons.