Past events

The brain is no longer considered a completely autonomous tissue with respect to its immune activity. Rather, immune surveillance is required for supporting brain functional plasticity and repair. Essential immune cells include the microglia, the resident immune cells of the brain, and circulating immune cells. Both the resident microglia and the circulating immune cells are under tight regulatory control to allow risk-free benefit from immunological interventions. We found that access of circulating immune cells to the brain is controlled by the brain’s epithelial barrier, the blood cerebrospinal barrier. Using immunological and immunogenomic tools, we discovered that in brain aging and under neurodegenerative conditions, this barrier does not optimally function to enable brain repair. We further showed in mouse models of Alzheimer’s disease (AD), that activating the immune system by immunotherapy directed against the inhibitory PD-1/PD-L1 immune checkpoint pathway drives an immune-dependent cascade of processes that start in the periphery and culminate with recruitment of monocyte-derived macrophages to the brain, which contribute to disease modification, reversing and slowing-down cognitive loss, reducing brain inflammation, and mitigating disease pathology in a mouse models of AD and Dementia (tauopathy). Overall, our results indicate that targeting the immune system outside the brain, rather than brain-specific disease-escalating factors within the central nervous system, can potentially provide a multi-dimensional disease-modifying therapy for AD and dementia.

Collective decision-making regarding direction of travel is observed during natural motion of animal and cellular groups. This phenomenon is exemplified, in the simplest case, by a group that contains two informed subgroups that hold conflicting preferred directions of motion. Under such circumstances, simulations, subsequently supported by experimental data with birds and primates, have demonstrated that the resulting motion is either towards a compromise direction or towards one of the preferred targets (even when the two subgroups are equal in size). However, the nature of this transition is not well understood. We present a theoretical study that combines simulations and a spin model for mobile animal groups. This allows us to identify the nature of this transition at a critical angular difference between the two preferred directions: in both flocking and spin models the transition coincides with the change in the group dynamics from Brownian to persistent collective motion. The groups undergo this transition as the number of uninformed individuals (those in the group that do not exhibit a directional preference) increases, which acts as an inverse of the temperature (noise) of the spin model. When the two informed subgroups are not equal in size, there is a tendency for the group to reach the target preferred by the larger subgroup. We find that the spin model captures effectively the essence of the collective decision-making transition and allows us to reveal a noise-dependent trade-off between the decision-making speed and the ability to achieve majority (democratic) consensus.

Primates live in large and complex social groups. It has been argued that this has led to evolutionary pressure on the brain and that there are networks that have been evolved to play an important role in social cognition and behaviors. Social deficits are widely known in many brain disorders such as autism and anxiety. Here we focused on two brain areas that were shown to play a crucial role in social interactions – the amygdala and the anterior-cingulate-cortex (ACC). Our goal was to understand the neural codes in these two regions and especially under social interactions: 1. Computational techniques that allow the comparison of on-going neural activity across these brain regions and species based on information theory measures was developed. We found that human neurons better utilize information capacity (efficient coding) than macaque neurons in both regions, and that ACC neurons are more efficient than amygdala neurons, in both species. In contrast, we found more overlap in the neural vocabulary and more synchronized activity (robustness coding) in monkeys in both regions, and in the amygdala of both species. Our findings demonstrate a tradeoff between robustness and efficiency across species and regions. We suggest that this tradeoff can contribute to the differential cognitive functions between species, and can underlie the complementary roles of the amygdala and the ACC. It can also contribute to the fragility underlying human psychopathologies. For more, see https://www.sciencedirect.com/science/article/pii/S0092867418316465 2. A novel electrophysiology experiment that induced real and live social interactions between humans and primates was conducted. In each daily session, we recorded neural responses in monkeys to the eye-gaze, direct or averted, of human intruders, and compared it with the responses to valence conditioning, aversive and appetitive. We found that the primate amygdala, but not the ACC, encodes eye-gaze; this coding is shared with valence coding through two mechanisms – “shared-activity” at the expectation epoch (conditioned stimulus, CS) and “shared-intensity” after the outcome (unconditioned stimulus, US). These shared mechanisms can open an indirect window for future therapy. For more, see https://www.biorxiv.org/content/10.1101/736462v1 3. We developed behavioral methods and algorithms to evaluate primates’ emotional states, using the analysis of facial expressions and a number of physiological parameters such as heart rate and respiratory rate. The primates’ emotional state evaluation will be the substrate for future studies that will investigate the neural correlates of these states.

For many decades, the neurobiological basis of language has been dominated by a conceptually dichotomous model in which speech perception is supported by Wernicke’s area in the temporal lobe and speech production is supported by Broca’s area in the frontal lobe. This model has been challenged by lesion and neuroimaging studies suggesting a more complex network of cortical structures supporting language. Many of the questions remaining in the field require a fine-grained temporal resolution together with spatial specificity in order to assay the dynamics of speech. Here I will introduce a series of studies employing direct electrocorticographic (ECoG) recordings in humans, illuminating the dynamics and cascade of neural events from perception to production of speech.