Fifth Annual SoFi Child Mind Institute Golf Invitational Raises $630,000 to Support Youth Mental Health 

San Francisco, CA – On April 20, the Child Mind Institute and SoFi held its fifth annual Golf Invitational at the Olympic Club in San Francisco. Participants included legendary athletes Marcus Allen (Los Angeles Raiders), Barry Bonds (San Francisco Giants), Royce Clayton (San Francisco Giants), Vince Coleman (St. Louis Cardinals), Al Joyner (Olympic gold medalist), Gary Payton (Miami Heat), and Sterling Sharpe (Green Bay Packers). The event raised $630,000 to support the organization’s mission to transform the lives of children and families struggling with mental health and learning disorders.

The day’s programming began with a round of golf where participants enjoyed time on the course alongside fellow supporters. Following the tournament, guests gathered for an evening reception and seated dinner highlighted by a live auction featuring exclusive experiences, and an awards presentation for tournament winners. The event featured remarks from Harold S. Koplewicz, MD, president of the Child Mind Institute, and Brian Boitano, Olympic gold medalist skater, who talked candidly about the mental pressures of performing on a global stage.

Raj Mathai, 12-time Emmy Award winner and NBC Bay Area weeknight news anchor, hosted the event and served as the dinner program emcee and auctioneer.

During the reception, the Child Mind Institute announced it is now seeing patients in a new San Francisco location, in addition to their San Mateo clinic, making it easier for families across the city, Marin County, and the northern East Bay to access care.

“Even as we grow our presence here in California, we know this challenge is bigger than any one location,” said Dr. Koplewicz. “If we’re going to meet the need, we have to reach children earlier in spaces where they already are: at home, in schools, in their communities, and increasingly, in the digital spaces where they spend so much of their time. Technology is already shaping young people’s lives. Our responsibility is to make sure it also supports them.”

“Supporting mental health is fundamental to building stronger families and more resilient communities,” said Anthony Noto, CEO of SoFi. “We’re proud to partner with the Child Mind Institute to expand access to critical mental health resources for children and families, helping empower the next generation to realize their ambitions and reach their full potential.”

Additional sponsors include Prologis, the Silk Family, GingerBread Capital, and Platform Golf, as well as product and vendor support from Bay Golf Club, Dryvebox, Drops of Dough, Goated Golf, Moretz Marketing, Sightglass Coffee, and Supergoop. Tracy Toyota served as the event’s Hole-in-One Sponsor.

The SoFi | Child Mind Institute Golf Invitational event committee included Stacy Denman, Ronnie Lott, Kristin Noto, and Linnea Roberts.

Photos are available upon request.


About the Child Mind Institute
The Child Mind Institute is dedicated to transforming the lives of children and families struggling with mental health and learning disorders by giving them the help they need. We’ve become the leading independent nonprofit in children’s mental health by providing gold-standard, evidence-based care, delivering educational resources to millions of families each year, training educators in underserved communities, and developing tomorrow’s breakthrough treatments.

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For press questions, contact our press team at childmindinstitute@ssmandl.com or our media officer at mediaoffice@childmind.org.

About SoFi
SoFi Technologies (NASDAQ: SOFI) is a one-stop shop for digital financial services on a mission to help people achieve financial independence to realize their ambitions. 13.7 million members trust SoFi to borrow, save, spend, invest, and protect their money and buy, sell and hold their crypto – all in one app – and get access to financial planners, exclusive experiences, and a thriving community. Fintechs, financial institutions, and brands use SoFi’s technology platform Galileo to build and manage innovative financial solutions across 128 million global accounts. For more information, visit www.sofi.com or download our iOS and Android apps.

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Bridging Countries and Building Capacity: A Bright Path Forward for Global Child Mental Health


By Peter Raucci, Director, Global Fellowships Strategy, Stavros Niarchos Foundation (SNF) Global Center for Child and Adolescent Mental Health at the Child Mind Institute


In May of 2025, I had the opportunity to visit Kenya to explore a possible expansion of the Stavros Niarchos Foundation (SNF) Global Center for Child and Adolescent Mental Health at the Child Mind Institute’s Clinical Fellowship model. Our goal was to build a new training pipeline connecting talented Kenyan clinicians with experts at the renowned Stellenbosch University in South Africa. The trip was eye-opening — not only because of the talent and dedication of the clinicians we met in Nairobi and Mombasa, Kenya’s two largest cities, but also because it reaffirmed a fundamental truth about global mental health. Collaboration across borders is essential.

This vision has now turned into a powerful reality. I’m proud to share that after identifying critical needs during the Kenya trip, we were able to select our first cohort of Fellows. These exceptional clinicians whose expertise, dedication, and deep commitment to their communities position them to be transformative leaders, are now on track to help pioneer this partnership.

Our inaugural fellows:

  • Muthoni Muthiga, psychiatrist
  • Milcah Olando, psychiatrist
  • Mercy Chege, psychologist

The plan is for the Fellows to spend a period of up to two years in South Africa and Kenya, receiving intensive training in child and adolescent mental health from the experts at Stellenbosch University. After concluding their Fellowship, all three have committed to continuing their work in Kenya’s public sector — exactly where their knowledge and skills are needed most.

SNF Global Center Clinical Fellows – Nairobi
SNF Global Center Clinical Fellows – Nairobi (left to right, top to bottom): Mercy Chege, Psychologist, Dr. Milcah Olando, Psychiatrist, Dr. Muthoni Muthiga, Psychiatrist

During the visit to Kenya, I witnessed an urgent and growing crisis in access to mental health care for youth. Through the SNF Global Center Fellowships Program, we aim to strengthen the capacity of the workforce by training local specialists like our inaugural Fellows. They can provide culturally responsive, evidence-based care while collaboratively building systems that prioritize youth mental health care.

Facilities like Kenyatta National Hospital and Mathari National Teaching and Referral Hospital in Nairobi — as well as public clinics in Mombasa County and Kilifi County — are in urgent need of CAMH specialists. For instance, in Kilifi County, only two psychiatric nurses serve a population of around 1.2 million people — leaving a staggering gap in mental health support for both youths and adults. Additionally, my conversations with clinicians at Aga Khan University (Kenya), a private institution with strong public partnerships that could serve as a vital hub for the Fellowship, further reinforced that sense of urgency. The clinicians I met are dedicated to improving outcomes for children and families. And what they need is time, training, mentorship, and the opportunity to grow into leadership roles in the field.

That’s why cross-country training opportunities like this matter. They don’t just build the skills of individual practitioners. They strengthen clinical networks, inspire new research, and ultimately transform systems of care. We are exploring ways to adapt our model to meet the unique needs and strengths of East and Southern Africa. Kenya has a fast-growing population of young people, yet trained CAMH specialists remain critically few. By training clinicians in South Africa and supporting their return to Kenya, we aim to help support a growing community of local experts working in public hospitals, university settings, and community mental health systems.

Ayesha Mian, MD, who sits on the Executive Council of the International Association for Child and Adolescent Psychiatry and Allied Professions (IACAPAP), joined me on the trip.

When reflecting on how much is being done in the field of global child and adolescent mental health, she says, “The answer must lie in disruptive solutions, collaborations, regional partnerships and cross disciplinary interventions that build and sustain systems. The partnership between Kenya and South Africa provides just such an opportunity, where the conversations ranged from on ground training of child and adolescent health care professionals to developing systems of care across the country and the region through policy, literacy, and capacity building.”

At the Serena Nairobi Hotel with attendees from Aga Khan University Nairobi, Stellenbosch University, IACAPAP, and health care and research representatives from across Kenya.

Partnerships between low- and middle-income countries (LMICs) and high-income countries (HICs) have the opportunity for impact. What’s just as powerful, perhaps even more transformative, are partnerships between LMICs themselves — countries where the economic, cultural, and systemic realities show evidence of pattern. South-South collaboration has the potential to build more contextually appropriate models of care with Fellows learning from mentors who understand the day-to-day realities of practicing in resource-constrained systems. Our Fellowship model has already proven successful in linking Mozambique with Brazil, where generalist clinicians receive training in child and adolescent mental health specializations.

This kind of collaboration isn’t about one-way knowledge transfer. It’s about co-creating solutions that are sustainable, regionally relevant, and driven by the people who will carry them forward. Over time, as this capacity grows, Kenya itself has the potential to become a regional hub for CAMH training — serving as a center of excellence for East Africa, including Uganda, Tanzania, and beyond.

The Fellowship model reflects the Child Mind Institute’s commitment to translating clinical excellence into scalable, global workforce solutions that strengthen public systems of care.

Learn more about the Global Fellowships Program

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Tideglusib improves novel object recognition memory in the preclinical DBA/2J mdx mouse model of Duchenne muscular dystrophy

IntroductionDuchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disorder characterized by progressive muscle wasting. Approximately 1 in 3 DMD patients experience cognitive dysfunction, with research suggesting an Alzheimer’s disease (AD)-like pathology. We have previously shown that treatment with the glycogen synthase kinase 3β (GSK3) inhibitor, tideglusib, improves muscle quality, function, and insulin sensitivity in the DBA/2J (D2) mdx mouse model of DMD. In this brief follow-up study, we report the effects of tideglusib treatment on cognitive function.MethodsMale D2 WT and mdx mice were purchased from Jackson Laboratories. Mice were separated into the following groups: (1) WT, (2) mdx-vehicle, and (3) mdx-tideglusib (10 mg/kg/day via oral gavage for 4 weeks). A novel object recognition test was performed to assess recognition memory. Hippocampus and serum samples were collected for BACE1 activity assays, amyloid beta (Aβ) ELISAs, and western blotting.ResultsCompared to vehicle-treated mdx mice, tideglusib-treated mdx mice demonstrated improved recognition memory. These changes to recognition memory were accompanied by greater expression of beta-catenin, an indirect downstream marker of GSK3 inhibition. While there were no changes in BACE1 activity, tideglusib-treated mdx mice had higher concentrations of Aβ in the serum and lower protein levels of receptor of advanced glycation end products.DiscussionThe results from this brief follow-up study offer preliminary support for tideglusib as a treatment for both muscle and brain impairments in mdx mice, potentially improving cognitive function through enhanced vascular Aβ clearance.

Expanding the phenotypic spectrum of Xq28 duplication involving MECP2: a familial case report

X-linked intellectual disability (XLID) is a well-recognized group of neurodevelopmental disorders, with pathogenic variants in X-chromosomal genes accounting for approximately 16% of intellectual disability cases in males. Clinical expression in females is variable and depends on patterns of X-chromosome inactivation. We describe three affected individuals from a single family with XLID caused by a confirmed duplication of the Xq28 region, including the genes SLC6A8, L1CAM, MECP2, TKTL1, FLNA, and GDI1. Two male siblings presented with severe phenotypes, including profound intellectual disability, severe speech impairment, behavioral issues, facial dysmorphism, spastic cerebral palsy, epilepsy, and cutaneous abnormalities. Their mother showed mild intellectual disability and skin manifestations. Family history suggested additional affected male relatives with a similar or even more severe clinical presentation. The duplication of multiple dosage-sensitive genes within the Xq28 region likely explains the multisystem involvement and the marked phenotypic variability observed between male and female family members. This report highlights the importance of considering Xq28 duplication, the most common X-linked copy number variation associated with intellectual disability, in the differential diagnosis of families with X-linked intellectual disability, especially if it is accompanied by additional neurological impairment.

Group CBT targeting hostile attribution bias in adolescents and young adults with ASD traits

BackgroundAdolescence is characterized by heightened self-consciousness and sensitivity to social evaluations. During this period, hostile attribution bias—interpreting ambiguous social cues as hostile—can lower quality of life (QOL) and contribute to future mental health problems. Adolescents with autism spectrum disorder (ASD) show similar difficulties, often more pronounced due to their cognitive style and interpersonal vulnerabilities. Group cognitive behavioral therapy (CBT) aims to correct such biases through structured cognitive and social experiences. This study evaluated the psychological effects of group CBT on hostile attribution bias, social functioning, and QOL in adolescents and young adults with ASD traits.MethodsWe conducted an 8-session group CBT program focusing on hostile attribution bias and suspiciousness in 21 adolescents and young adults with ASD traits attending a hospital psychiatric outpatient department. The 15 participants who completed the program were included in analyzes. Psychological indices included hostile attribution bias (Ambiguous Intentions Hostility Questionnaire), social functioning (Social Responsiveness Scale, Second Edition [SRS-2]), and subjective QOL. Pre–post changes were quantified as change rates ((post − pre)/pre × 100). Group-level changes were tested with paired analyzes; exploratory associations among change rates were examined using Spearman correlations.ResultsGroup CBT significantly improved hostile attribution bias (effect size [ES] = 0.698, p = 0.017), social communication and interaction (SRS-2; ES = 0.780, p = 0.012), and subjective QOL (ES = 0.752, p = 0.011). Exploratory individual-level analyzes showed a discordant pattern: smaller reductions in hostile attribution bias (less negative change rates) were associated with greater increases in subjective QOL (ρ = 0.597, p = 0.019).ConclusionsThis pilot study suggests that group CBT may reduce hostile attribution bias and improve QOL and social functioning in adolescents and young adults with ASD traits. Notably, the positive correlation between hostile attribution bias change rates and QOL change rates suggests that greater QOL gains were not necessarily accompanied by larger reductions in hostile attribution bias, indicating that improvements in cognitive bias and perceived well-being may arise through partly distinct or non-linear pathways rather than a simple one-to-one relationship.Clinical trial registryUniversity Hospital Medical Information Network (UMIN000030140).

GABA-Based Target for Alzheimer’s Therapy Identified

Researchers at the University of Galway have found evidence that targeting inhibitory signaling in the brain may help address cognitive dysfunction in Alzheimer’s disease (AD), a finding that runs counter to current therapeutic approaches that focus on influencing excitatory pathways. The research, published in Neuropharmacology, identifies how modulation of gamma-aminobutyric acid (GABA) signaling can restore disrupted neural balance and improve memory-related function in AD disease models.

“Given the ever-increasing burden of Alzheimer’s disease, the urgent need for the identification of novel targets for the development of disease-modifying therapy is clear,” said senior author Andrea Kwakowsky, PhD, associate professor of pharmacology and lead researcher at the School of Medicine, University of Galway.

Alzheimer’s disease is characterized by progressive cognitive impairment and is associated with hallmark pathological features including β-amyloid (Aβ) plaques and neurofibrillary tangles. In addition to these, disruption of the brain’s excitatory/inhibitory (E/I) balance has gained traction as a central mechanism contributing to memory loss. Today, most approved therapies for AD target excitatory neurotransmitter systems such as cholinergic and glutamatergic pathways, but “the symptomatic relief provided by these therapies is only marginal, and the progression or underlying causes of the disease are not addressed,” the researchers noted.

For their work, the University of Galway team instead focused on the inhibitory side of this balance, specifically the role of gamma-aminobutyric acid (GABA), the brain’s main inhibitory neurotransmitter. GABA regulates neuronal activity and is essential for maintaining stable network function and memory processes. In AD, however, E/I balance becomes dysregulated with increased extracellular GABA—triggered in part by Aβ—leading to overactivation of certain GABA receptors, particularly α5-containing GABA type A receptors (α5-GABA ARs), which are abundant in the hippocampus. The result is a dampening of neuronal signaling and which impairs learning and memory.

“Our research is significant in that it demonstrates that if we block this GABA receptor activity in nerve cells we can reverse Alzheimer-like effects caused by amyloid beta and improve cognitive performance,” Kwakowsky said.

To test whether blocking a5-GGABA A could help restore E/I balance, the team investigated α5IA, an α5-GABA AR-selective inverse agonist. α5IA works by reducing the activity of α5-GABA ARs, which decreases excess tonic inhibition. The data showed that in experimental models of AD, the compound improved long-term potentiation (LTP), a mechanism of synaptic plasticity and memory, reduced abnormal inhibitory conductance, and restored spatial memory performance.

Mechanistically, α5IA appears to act by restoring physiological levels of inhibition in the hippocampus which is critical for memory formation. By reducing excessive tonic inhibition, it rebalances E/I signaling, which allows neuronal circuits to function more effectively. “The data presented here suggest that in both ex vivo and in vivo AD models, α5IA improves cognitive function by restoring CA1 tonic inhibition, thereby re-establishing E/I balance and ameliorating the abnormal hippocampal network activity induced by Aβ1-42,” the researchers wrote.

This new study is the latest to indicate that targeting inhibitory neurotransmission could be an effective treatment approach for AD. Earlier research has shown that α5-GABA AR modulation enhances memory and reduces inhibitory signaling in both animal models and humans. But most of these studies have not directly examined the effect of α5IA in chronic neurodegenerative disease models.

The researchers noted there are some limitations to their work, pointing out that while α5IA improved cognitive outcomes, it did not reverse neuronal loss in vivo, suggesting that its effects may be primarily functional rather than neuroprotective at later stages of AD. Also, variability in drug exposure and timing may influence outcomes. Finally long-term use of α5IA has also been associated with safety concerns at high doses, including renal toxicity, so further research is needed to determine toxicity and dosing regimens and limits.

Nonetheless, the implications of this research indicate there is potential to develop new AD therapies that directly target network dysfunction rather than focusing solely on amyloid accumulation or excitatory signaling. By restoring E/I balance, this approach shows the potential to improve cognitive function even when AD pathology has taken root. The findings could also benefit diagnostic methods, as biomarkers of inhibitory dysfunction or altered GABA signaling could help identify patients who would benefit an approach that rebalances E/I signaling.

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Number of children and maternal mental health in the context of China’s fertility policy transition: the moderating effect of employment status and the mediating effect of family environment

BackgroundHaving more children may be detrimental to maternal mental health during China’s ongoing fertility policy transition. However, under what circumstances and how number of children could be associated with maternal mental health remains understudied in China. This study examined the association between number of children and maternal anxiety and depressive symptoms among mothers of middle school students in Shanghai, China. It also explored the moderating effect of maternal employment status and the mediating effect of family environment.MethodsMothers of students from 7 middle schools in Shanghai were surveyed. In total, 4,215 valid questionnaires were obtained. The survey included sociodemographic information, the Generalized Anxiety Disorder Scale (GAD-7), the Center for Epidemiologic Studies Depression Scale (CES-D), and the Chinese version of the Family Environment Scale (FES-CV). Multiple linear regression analysis was performed to examine the association between number of children and maternal anxiety/depressive symptoms. Model 1 and Model 4 of SPSS PROCESS were then employed to examine the moderating effect of employment status and the mediating effect of family environment.ResultsThe rates of clinically significant anxiety and depressive symptoms among mothers were 13.6% and 17.6%, respectively. The moderating effect of maternal employment status was significant. Among unemployed mothers, number of children was positively associated with both maternal anxiety and depressive symptoms, whereas among employed mothers, number of children was not associated with maternal anxiety or depression. Among unemployed mothers, family environment mediated the association between number of children and maternal anxiety/depressive symptoms through the pathways of family conflict and organization. Among employed mothers, family environment suppressed the association between number of children and maternal anxiety/depressive symptoms through the pathways of family conflict, intellectual-cultural orientation, organization, control, and independence.ConclusionOur findings suggest that number of children per se is not necessarily associated with worsened maternal mental health. Instead, the potential changes in employment participation and family environment that accompany having more children may be more relevant. Therefore, stakeholders, clinicians, and researchers should therefore focus on these aspects when addressing maternal mental health.