Scientists are rethinking how depression should be treated by focusing less on reducing negative feelings and more on rebuilding the brain’s capacity for positive emotion.
From a cellular perspective, senescence has been considered a binary state, wherein cells are either senescent or not. This reductionist notion, often defined as irreversible growth arrest, has guided efforts to identify universal biomarkers and senolytics, but both have consistently eluded us. This outcome is not surprising, given that the biological nature of senescence may not be strictly irreversible; the accumulated evidence suggests that growth arrest can become unstable over time, with cells acquiring alterations, occasionally regaining proliferative capacity, or undergoing partial reprogramming, and exhibiting a heterogeneous spectrum of phenotypes (“senotypes”) influenced by tissue types, stressors, temporal dynamics, and disease states.
Our memories of past events are typically not isolated, but they are linked to other related memories. This ability to establish connections between related memories is highly advantageous, as it helps us to recognize familiar patterns in new situations and make predictions that can inform our decisions.
Researchers at UCLA’s Brain Research Institute recently carried out a study on mice aimed at better understanding how the brain decides what memories are connected and which ones are not. Their paper, published in Nature Neuroscience, pinpoints brain regions that could play a role in the organization of memories into coherent pools of knowledge.
“Our lab has long been interested in understanding how the brain connects related memories,” André F. de Sousa, first author of the paper, told Medical Xpress. “In everyday life, new experiences are rarely processed in isolation. Instead, they are often shaped by what we have learned before. This ability allows us to link related events, build knowledge, and use past experiences to guide future behavior. However, this process needs to be carefully controlled.”
A novel, noninvasive brain stimulation approach—known as transcranial temporal interference stimulation (TIs)—may offer a new way to treat motor symptoms in Parkinson’s disease without the need for surgery, according to a pilot study appearing in eBioMedicine. The technique, which uses overlapping electrical currents to selectively target deep brain regions, significantly improved movement in patients compared with a sham treatment when targeting the subthalamic nucleus.
Parkinson’s disease is a progressive neurological disorder that affects movement, often causing tremor, stiffness, and slowed motion. One of the most effective treatments for advanced symptoms is deep brain stimulation (DBS), which involves implanting electrodes into the brain. TIs may be able to achieve a similar effect—targeting the same deep brain structures —but entirely from outside the skull, using carefully calibrated electrical fields delivered through the scalp.
In the randomized, double-blind, crossover study, titled “Transcranial temporal interference stimulation targeting the subthalamic region for motor symptoms in Parkinson’s disease: a pilot, randomised, double-blind, sham-controlled crossover study,” 30 people with early-to mid-stage Parkinson’s disease received a single 20-minute session of individualized TIs targeting the subthalamic region—a key node in the brain’s motor control network—as well as a sham or placebo treatment in a separate session.
For many people who smoke, quitting is not just a matter of willpower. It is a tug-of-war in the brain—between the pull of reward and the ability to resist.
A study published in the Journal of Psychiatric Research suggests that shifting that balance may be possible. Using a noninvasive brain stimulation technique called repetitive transcranial magnetic stimulation, or rTMS, researchers at MUSC Hollings Cancer Center found that stimulating a specific brain region that regulates self-control significantly reduced how much people smoked.
Lin et al. reveal that tumor-infiltrating bystander CD8+ T cells are heterogeneous and undergo a TCM-to-TEM-to-TRM differentiation trajectory driven by Treg-derived TGF-β signaling through suppression of KLF2. This mechanism sustains bystander CD8+ T cell heterogeneity and accumulation in tumors and provides a targetable mechanism for cancer immunotherapy.