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Immune therapy for Alzheimer’s takes a step forward: Phase I trial reports positive results

Dozens of research teams around the world are working to halt, treat and even prevent Alzheimer’s disease, which silently develops in the brain for more than a decade before symptoms appear. Although recent years have brought important advances, researchers continue to search for therapies that can more effectively alter the course of Alzheimer’s and other forms of dementia.

Professor Michal Schwartz of the Weizmann Institute of Science’s Brain Sciences Department has developed an innovative strategy for treating Alzheimer’s disease. A recipient of the Israel Prize in Life Sciences, Schwartz pioneered research showing that the body’s most protected organ—the brain—is tightly dependent on the immune system for its lifelong functioning, maintenance and repair.

These findings overturned the long-held dogma that the brain was entirely isolated from immune activity and that any immune activity within the brain was inherently detrimental and should therefore be suppressed.

Prognostic Value of Blood-Based P-Tau217 Levels for Progression to Cognitive Impairment

This cohort study examines the absolute risk of progression to cognitive impairment and rates of cognitive decline per the blood-based biomarker plasma phosphorylated tau 217 (p-tau217) among cognitively unimpaired older adults.

The future of neurotechnology | Sri Sarma | TEDxBoston

NOTE FROM TED: This talk only represents the speaker’s personal approach to and understanding of neural systems, technology, and defense. TEDx events are independently organized by volunteers. The guidelines we give TEDx organizers are described in more detail here: http://storage.ted.com/tedx/manuals/t

Autonomous systems can process vast amounts of information—but they struggle when the unexpected happens. The human brain, by contrast, thrives in uncertainty. In this provocative talk, Sri Sarma reveals how merging machine intelligence with living neural systems could create a new class of adaptive technologies, from resilient autonomous vehicles to precision therapies that operate inside the human body. The nations that lead this future in \.

Two hours of sleep restored: Researchers make Alzheimer’s breakthrough

There’s a small fire isolated in your kitchen. If you had the right tool, you might be able to put it out. But before you can, the sprinklers turn on and flood your entire house. An automatic response to an issue has now damaged everything you own.

That’s akin to what happens in the brains of people with Alzheimer’s: Amyloid plaques, sticky protein clumps that build up in the brain, are the fire in the kitchen. Microglia, the brain’s resident immune cells, are the sprinklers. A mechanism designed to protect the body ends up hurting it.

Researchers at the University of Kentucky have discovered this harmful process for the first time—and figured out how to turn it off.

Postnatal Development of Pyramidal Neurons Excitability and Synaptic Inputs in Mouse Gustatory Cortical Circuits

During postnatal development, mammals shift from relying on their mother’s milk to foraging for food. Early experience with feeding independence influences the development of taste preferences (Schiff et al., 2023). While the postnatal development of gustatory cortical circuits is not well studied, there is some experimental evidence for protracted maturation of neuronal morphology and early-life experience-dependent effects on neurons in other regions of the taste system. In mice, taste receptor cells begin to reliably fire action potentials during the third postnatal week (Bigiani et al., 2002) and the refinement of their excitability extends into adulthood (Bigiani et al., 2002; Ohtubo et al., 2012). Postnatal anatomical rewiring was observed in the first central relay in the gustatory system, the nucleus of the solitary tract (NTS) after postnatal day 21 (P21), with the inputs to the NTS reaching adult connectivity by P35 and undergoing additional refinement into adulthood (Hill et al., 1983; Sollars et al., 2006; May et al., 2008; Sun et al., 2017). In the gustatory portion of the parabrachial nucleus, dendritic arborization of multipolar and fusiform cells reach adult morphology by P35 (Lasiter and Kachele, 1988). Together, these studies identify the postnatal window between P15–P21, P21–P35, and P50–P65 as periods of maturation for different circuits in the gustatory system.

In primary visual, auditory, and somatosensory cortices, developmental time windows of heightened sensitivity to changes in sensory inputs extending between the third and fifth postnatal week have been identified (Micheva and Beaulieu, 1995; Antonini et al., 1999; Maffei et al., 2006, 2010; Maffei and Turrigiano, 2008b; Wang et al., 2011; Takesian et al., 2012, 2018; Gainey and Feldman, 2017; Gainey et al., 2018). During these periods, known as critical periods, cortical circuits undergo a maturation process that is shaped by experience and reach their adult properties.

GABAergic inhibitory synapses in particular play a crucial role in postnatal cortical circuit maturation and refinement. Inhibitory cortical circuits themselves undergo extended postnatal maturation (Hensch, 2004; Tatti et al., 2017; Takesian et al., 2018), with increases in GABAergic inhibition opening the critical period for circuit refinement. For instance, in a knock-out mouse in which GABA is severely diminished (GAD-KO), the critical period may never open unless GABA receptors are activated pharmacologically (Fagiolini and Hensch, 2000). Changes in inhibitory circuits during critical periods are primarily ascribed to parvalbumin-expressing interneurons (PV+ INs). Reports show an increase in the number of PV+ INs (Gonchar et al., 2007; Tatti et al., 2017) along with increased perisomatic innervation of pyramidal neurons (Chattopadhyaya et al., 2004). This process is associated with increases in the expression of PV in PV+ INs (Murase et al.

New mechanism explains how spinal stimulation improves arm movement after stroke

Researchers in the Neuromechatronics Lab at Carnegie Mellon University have already proven that spinal cord stimulation can help people regain movement after stroke, but until now they didn’t quite know how.

In a new study, published today in Cell Reports Medicine, a research team led by Doug Weber, professor of mechanical engineering and neuroscience, and Ph.D. candidate Luigi Borda report that epidural spinal cord stimulation works by restoring inhibitory spinal circuits. These circuits enable the nervous system to coordinate opposing muscles, such as the biceps and triceps, which must work together to bend and straighten the elbow. After a stroke, those neural control circuits are disrupted. The new study found that spinal cord stimulation helps restore that balance, allowing stroke survivors to move their arms more smoothly, quickly and efficiently.

“This discovery allows us to move beyond simply strengthening weak muscles; we can now fine-tune stimulation to release the ‘brakes’ on overactive muscles, providing a more effective and personalized path to recovery,” said Weber.

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