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Unexpected finding could offer new treatment targets for meth addiction

University of Florida neuroscientists have made a mechanistic discovery that paves the way to test immune-modulating medicines as a potential tool to break the cycle of methamphetamine addiction.

In a new preclinical study, a McKnight Brain Institute team led by Habibeh Khoshbouei, Ph.D., Pharm. D., examined the role of neuroinflammation in meth addiction to provide a deeper understanding of the mechanisms at work.

“Unlike alcohol or opioids, there currently is no medicinal therapeutic approach for methamphetamine addiction,” said Khoshbouei, a professor of neuroscience and psychiatry. “So this is an important societal issue.”

Two wrongs make a right: How two damaging disease variants can restore health

Scientists at Pacific Northwest Research Institute (PNRI) have overturned a long-held belief in genetics: that inheriting two harmful variants of the same gene always worsens disease. Instead, the team found that in many cases, two harmful variants can actually restore normal protein function.

Their work appears in the Proceedings of the National Academy of Sciences.

Scientists report new immune insights and targets into LRRK2 mutations in Parkinson’s disease

Parkinson’s disease (PD) is a debilitating and progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra, a brain region essential for motor control. Clinically, it is marked by tremor, rigidity, bradykinesia and postural instability, symptoms that progressively erode independence and quality of life.

PD affects millions of people worldwide, including nearly one million individuals in the United States, making it one of the fastest-growing neurological disorders. In the U.S. alone, the disease imposes a profound health care and socioeconomic burden, with annual costs reaching tens of billions of dollars due to medical care, lost productivity and long-term disability.

While environmental factors contribute to disease risk, genetic drivers are increasingly recognized, with mutations in the leucine-rich repeat kinase 2 (LRRK2) gene representing one of the most common causes of both familial and sporadic PD. Understanding how LRRK2 mutations drive disease is therefore central to developing therapies that go beyond symptoms control.

Tissue repair slows in old age. These proteins speed it back up

As we age, we don’t recover from injury or illness like we did when we were young. But new research from UCSF has found gene regulators—proteins that turn genes on and off—that could restore the aging body’s ability to self-repair.

The scientists looked at fibroblasts, which build the scaffolding between cells that give shape and structure to our organs.

Fibroblasts maintain this scaffolding in the face of normal wear, disease, and injury. But over time, they slow down, and the body suffers.

Association Between Circadian Rest-Activity Rhythms and Incident Dementia in Older AdultsThe Atherosclerosis Risk in Communities Study

Weaker and more fragmented circadian rest-activity rhythms and later peak activity time were associated with elevated dementia risk in this study.

First Therapy Chatbot Trial Yields Mental Health Benefits

face_with_colon_three Year 2025


Dartmouth researchers conducted the first-ever clinical trial of a generative AI-powered therapy chatbot and found that the software resulted in significant improvements in participants’ symptoms, according to results published March 27 in NEJM AI.

People in the study also reported they could trust and communicate with the system, known as Therabot, to a degree that is comparable to working with a mental health professional.

The trial consisted of 106 people from across the United States diagnosed with major depressive disorder, generalized anxiety disorder, or an eating disorder. Participants interacted with Therabot through a smartphone app by typing out responses to prompts about how they were feeling or initiating conversations when they needed to talk.

Autologous T cell therapy targeting multiple antigens shows promise in treating pancreatic cancer

A recent publication in Nature Medicine describes a novel immunotherapy targeting pancreatic cancer that has shown promising results in a first in-human phase 1/2 trial.

The TACTOPS trial, which investigated the safety and clinical effects of autologous T cell therapy targeting multiple tumor antigens, was a collaboration among researchers at Baylor College of Medicine, the Dan L Duncan Comprehensive Cancer Center, the Center for Cell and Gene Therapy, Texas Children’s Hospital and Houston Methodist Hospital.

“We wanted to develop a targeted therapeutic that would hone the immune system on tumor-associated antigens (TAAs) that were present on malignant cells. We targeted five different antigens to deal with the polyclonal nature of the disease,” said co-corresponding author Dr. Ann Leen, professor of pediatrics–hematology and oncology in the Center for Cell and Gene Therapy.

Pediatric Cohort of Charcot-Marie-Tooth DiseaseClinical Features and Genetic Distribution

This study represents a characterization of pediatric Charcot-Marie-Tooth disease in a Canadian cohort and demonstrates that disease onset, severity, and manifestations are highly variable even in childhood.


Background and Objectives.

Opposing functions of distinct regulatory T cell subsets in colorectal cancer

For this study, the researchers focused on a type of colorectal cancer that accounts for 80% to 85% of all colorectal cancers — microsatellite stable (MSS) with proficient mismatch repair (MMRp), meaning the tumors’ DNA is relatively stable. These cancers are largely resistant to checkpoint inhibitor immunotherapies.

Previous groundbreaking research found checkpoint inhibitors alone could successfully treat rectal cancer and several other cancers with the opposite tumor type — those with high microsatellite instability (MSI-H) and mismatch repair deficiency (MMRd). This allows doctors to spare many patients from surgery, chemotherapy, and radiation.

Here the team employed an mouse model that accurately recreates the common mutations, behaviors, and immune cell composition of human colorectal cancer. They found that the regulatory T cells associated with the cancer are split between two types: Cells that make a signaling molecule (cytokine) called interleukin‑10 (IL-10) and cells that don’t.

Through a series of sophisticated experiments that selectively eliminated each type of cell, the researchers discovered:

When IL-10-positive cells were removed, tumor growth accelerated.


In most solid tumors, high numbers of regulatory T (Treg) cells are associated with poorer outcomes because they dampen the immune system’s ability to fight against a tumor.

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