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Immune molecule long tied to inflammation may benefit the aging brain

Inflammation in the brain is usually seen as harmful in the aging process—it’s thought to contribute to Alzheimer’s and dementia. But a new study in mice suggests that inflammation, led by an immune molecule called STING (stimulator of interferon genes), might have a role in protecting the aging brain. The findings also have implications for new experimental Alzheimer’s drugs that are designed to block STING.

For the study published in Cell Reports, scientists at Tufts University School of Medicine examined brain function, inflammation, and movement in genetically engineered to lack STING, compared with normal controls. They found that mice without STING had worse memory and movement problems, mimicking the senility and frailty seen in people with dementia and Alzheimer’s disease.

“Our data suggest that the that STING supports may actually be necessary for the brain to stay healthy and in balance during old age,” says Shruti Sharma, an assistant professor of immunology at Tufts University School of Medicine and the study’s senior author.

Mirtazapine for Methamphetamine Use Disorder: A Randomized Clinical Trial

In adults with methamphetamine use disorder, mirtazapine reduced methamphetamine use by approximately two more days per month vs placebo, with no unexpected safety concerns.


Main Outcomes and Measures The primary end point was the change in days of methamphetamine use in the past 28 days from baseline to week 12. Secondary end points were depression, insomnia, HIV risk behavior, quality of life, and methamphetamine-negative oral fluid samples.

Results Of 344 participants randomized, 339 participants received the intervention (167 in the placebo group and 172 in the mirtazapine group). Mean (SD) age was 42.0 (8.6) years, 126 participants (37.2%) were female, and participants had used methamphetamine for a median (IQR) of 24 days (17−28) of the past 28 days at baseline. The mean reduction in days of methamphetamine use from baseline to week 12 was greater in the mirtazapine group (7.0 days of 28 days) than in the placebo group (4.8 days of 28 days; mean difference, 2.2 days; 95% CI, −4.2 to −0.2 days; P = .02). More participants in the mirtazapine group reported drowsiness (47% vs 33%) and weight gain (10% vs 3%). Forty participants (23%) discontinued mirtazapine due to adverse events compared to 25 participants (15%) in the placebo group. No significant effects of mirtazapine on secondary end points were found.

Conclusions and Relevance In this parallel-group randomized clinical trial, mirtazapine delivered in routine clinical practice reduced methamphetamine use in adults with methamphetamine use disorder. No unexpected safety concerns delivering mirtazapine in this setting were found; this finding has important clinical implications in the absence of any approved pharmacotherapies for methamphetamine use disorder.

The frequency-dependent effects of primary hand motor cortex stimulation on volitional finger movement

[Brain stimulation] Taquet et al.: “The effect of motor cortex stimulation on finger flexion is frequency dependent.”


We conducted a prospective study in human patients undergoing awake craniotomies to examine whether the effects of cortical stimulation in hand primary motor cortex (M1) can be frequency dependent and inhibitory.

In 11 participants undergoing clinically indicated awake craniotomies, we delivered bursts of 1–333 Hz stimulation during a finger-flexion task. Synchronized electrocorticography (ECoG), finger joint kinematics, electromyography (EMG), and video were recorded.

Inability to flex the index finger during subthreshold stimulation was noted in 3 participants at frequencies 250 Hz when the electrodes were in locations that induced extension of the forefinger at higher amplitudes. Other than these trials, all stimulation events either induced muscle contractions or had no measurable effect.

A hidden DNA region helps drive frailty, exposing brain and immune links that reshape aging risk

Researchers at McMaster University have identified, for the first time, a novel region of DNA and two associated genes connected to frailty, offering neurological and immune-related insights that might help explain why some older adults are more likely to be frail than others.

The McMaster team’s findings, published in the journal npj Aging, fill an important gap by revealing genetic factors that contribute to the development of frailty. The discovery provides a biological connection to the condition and points toward new avenues for early detection and targeted intervention.

Cellular and molecular landscapes of human tendons across the lifespan revealed by spatial and single-cell transcriptomics

Kurjan et al. map human tendon architecture from embryo to adult using spatial and single-cell transcriptomics. They show embryonic progenitors generate fibrillar, connective, and chondrogenic tendon lineages. Fibroblasts reprogram with age, whereas immune, vascular, and neural cells remain stable. Ruptured adult tendons partially reactivate fetal programs without full regeneration.

Microfluidic chip reveals how living glioblastoma slices resist chemotherapy

Combining microchip engineering techniques with cutting-edge gene profiling, scientists at Columbia University have developed a new way to study drug responses in living slices of human brain tumor cells. The system, using a type of chip called a microfluidic device, has already revealed new details about how these aggressive tumors resist chemotherapy drugs and could help researchers develop more effective treatments.

The work grew from earlier efforts to study glioblastoma tumors removed from patients during surgery. “These samples that we’re getting from our colleagues who resect these tumors clinically, they’re alive, and we can actually do experiments directly on those surgical samples,” says Peter Sims, Ph.D., associate professor of systems biology at Columbia and senior author on the new study, which appears in the journal Lab on a Chip.

Benefits and Harms of Dementia Screening for Family Members of Older Adults: A Randomized Clinical Trial

Alzheimer disease and related dementias screening of adults ≥65 years in primary care had no significant benefits or harms on family member quality of life or psychological well-being.


Question How does screening adults aged 65 years and older for dementia in primary care affect their family members’ health-related quality of life, stress, and perceived readiness to provide care?

Findings In this randomized clinical trial that included 1808 patient-family member dyads, there was no significant difference in benefit of screening to family members, measured by physical and mental component summary scores, and no difference in harm, measured by depression and anxiety between the screen and no screen groups over time.

Meaning These findings suggest that screening older adults for dementia in primary care did not improve or worsen their family members’ quality of life or psychological well-being.

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