The functional capacities of a biosensor depend on the number of surrounding neurons in a given radius (50–350 μm) (He et al., 2020). Probe insertions generate inflammatory responses to acute tissue injuries and the introduction of foreign bodies, known as “foreign body response” (FBR). Chronic neuroprosthetic implants in rats at 16 weeks in contrast to 8 weeks have been shown to increase neuronal and dendritic loss, correlate with tau hyperphosphorylation seen in Alzheimer's disease and other tauopathies, and impede regeneration and recording of activity surrounding the device (McConnell et al., 2009). Assessments of acute proinflammatory events and chronic progression have largely centered on histological analyses of non-neuronal central nervous system (CNS) cells such as microglia, astrocytes and oligodendroglia, including their contribution to neuroinflammation and glial scars (Kozai et al., 2015; Prodanov and Delbeke, 2016).

Ischemic stroke and cerebral venous thrombosis are both leading causes of disability. Both involve plasmatic coagulation, platelets, and immune cells, but pathomechanisms differ. Stroke is a thrombo-inflammatory disease with immune cell recruitment and barrier breakdown. Cerebral venous thrombosis is caused by thrombotic occlusion of cerebral veins and is a prime example of immunothrombosis.

A fine fiber catheter was implanted in rat brain together with a flexible polyimide microelectrode in sight both of which acts as a foreign body and induces the brain tissue immune reaction. OCT signals were collected from animals up to 12 weeks after implantation and thus gliotic scarring in vivo monitored for that time. Preliminary data showed a significant enhancement of the OCT backscattering signal during the first 3 weeks after implantation, and increased attenuation factor of the sampled tissue due to the glial scar formation.

Key design considerations for biocompatibility, efficacy and longevity of microelectrodes to maintain long-term neuronal recording and stimulation are highly dependent on brain tissue response (Polikov et al., 2005). The functional capacities of a biosensor depend on the number of surrounding neurons in a given radius (50–350 μm) (He et al., 2020). Probe insertions generate inflammatory responses to acute tissue injuries and the introduction of foreign bodies, known as “foreign body response” (FBR). Chronic neuroprosthetic implants in rats at 16 weeks in contrast to 8 weeks have been shown to increase neuronal and dendritic loss, correlate with tau hyperphosphorylation seen in Alzheimer's disease and other tauopathies, and impede regeneration and recording of activity surrounding the device

Contrary to the initial hypothesis, dual targeting worsened the neuroinflammatory response to intracortical probes. Therefore, probe material and CD14 deficiency were independently assessed for their effect on inflammation and neuronal density by implanting each microelectrode type in both wild-type control and Cd14-/- mice.

Fractalkine (CX3CL1) has unique properties as an adhesion molecule and chemoattractant, and by acting on its only receptor, CX3CR1, it regulates the activity of microglia in physiological states and neuroinflammation. Depending on the clinical context, CX3CL1-CX3CR1 signaling may have neuroprotective effects by inhibiting the inflammatory process in microglia or, conversely, maintaining/intensifying inflammation and neurotoxicity.

Dubbed the Prima, the implant consists of a 2-mm square chip that is surgically placed under the retina, the backmost part of the eye, in an 80-minute procedure. A pair of glasses with a camera captures visual information and beams patterns of infrared light on the chip, which has 378 light-powered pixels. Acting like a tiny solar panel, the chip converts light to a pattern of electrical stimulation and sends those electrical pulses to the brain. The brain then interprets those signals as images, mimicking the process of natural vision.

Nowadays, the mHealth market is flooded with smartphone applications (apps) lacking validation for blood pressure (BP)-lowering effects and BP measurement accuracy. This systematic review for Guidelines for BP control using digital technologies of the Japanese Society of Hypertension aimed to assess the validation studies of apps.

Breakdown of the blood-brain barrier (BBB) and increased immune cell trafficking into the central nervous system (CNS) are hallmarks of the pathogenesis of multiple sclerosis (MS). Platelet endothelial cell adhesion molecule-1 (PECAM-1; CD31) is expressed on cells of the vascular compartment and regulates vascular integrity and immune cell trafficking. Involvement of PECAM-1 in MS pathogenesis has been suggested by the detection of increased levels of soluble PECAM-1 (sPECAM-1) in the serum and CSF of MS patients.

Elad Levy will present results of the clinical trial that assessed the safety of Synchron’s endovascular brain-computer interface in people with severe paralysis at the Congress of Neurological Surgeons (CNS).

La solution de Remedee Labs, reposant sur le premier bracelet stimulateur d’endorphines à base d’ondes millimétriques, devient le premier dispositif médical validé cliniquement et certifié en Europe pour soulager les symptômes de la fibromyalgie, une maladie pour laquelle aucun traitement spécifique n’avait encore été indiqué jusqu’à présent. Remedee Labs lancera sur le marché en 2025 son offre médicale dédiée aux personnes atteintes de fibromyalgie.

Brain signals reflect the handled activities and controlling behavior of the brain or the influence of the received information from other body parts either sensing or internal organs. Brain Computer Interfacing provides a channeling facility between brain and external equipment.

Gene sequence could be implanted with electrodes to make neurons larger and easier to ‘read’ in quest for better mind control of devices

The first implanted brain-computer interface has been turned on in the US. It allows a person to control a computer using only their thoughts. Though the tech is clunky, it could one day be used by astronauts and military personnel.

Humans controlling machines with their minds may sound like something from a sci-fi movie, but it’s becoming a reality through brain-computer interfaces. Understanding this emerging technology now can help ensure that effective policies are in place before BCI becomes a part of everyday life.

The findings, reported Sept. 1 at the European Society of Cardiology meeting and published in the Journal of the American College of Cardiology, provide inconclusive data about whether atrial fibrillation screening lowers stroke rates. The COVID pandemic led to an early halt of the study before fully enrolling, so it did not have enough participants to establish definitive results about stroke.

The controversial company said its second human patient is using the device to design 3D objects and play video games, while issues with the first patient’s device have been fixed.

Alex’s implant marks the second time Neuralink has successfully implanted its BCI into a patient. Earlier this year, Neuralink implanted it into Noland Arbaugh, a quadriplegic. According to the company, he controlled a computer cursor and played video games with the BCI. However, soon after receiving the implant, several threads from the BCI retracted from Mr. Arbaugh’s brain, significantly reducing the device’s capabilities. While the issue has been rectified, the malfunction raised concerns about the safety of Neuralink’s technology.

The company behind this, Inner Cosmos, calls their BCI a “Digital Pill for the Mind”; about the size of a penny, this wearable delivers precise micro-stimulations, similar to TMS, but without the need to visit a hospital for weeks in a row, or interact with the traditional machinery in the hospital setting. That is a game-changer in terms of the time, effort and cost of providing care or accessing treatment.

In a tissue culture model of the blood–brain barrier, antagonizing the interaction of CD200 and sCD200 with T-cell CD200 receptor (CD200R1) via anti-CD200 blocking antibodies or the RNAi-mediated inhibition of CD200 production by endothelial cells increased T-cell adhesion and transmigration across monolayers of endothelial cells. Our findings demonstrate that sCD200 produced by brain endothelial cells regulates immune cell trafficking through the blood–brain barrier and is primarily responsible for preventing activated T-cells from entering the brain.