All articles tagged with #schizophrenia
Large-scale analyses of over 1 million people across 14 psychiatric conditions identify five shared genetic signatures that drive most risk, with schizophrenia and bipolar disorder sharing about 70% of their genetic signal. The findings suggest common biological pathways across disorders, challenging traditional separate diagnoses and hinting at unified treatments targeting pleiotropic genetic factors.
A 30-year-old sister wrestles with the prospect of becoming her 34-year-old brother’s legal guardian after their father’s death. She loves him but doubts her ability to make life-changing decisions for him, aware that refusing could make him a ward of the state, while acknowledging his need for steady professional care.
Rohinie Bisesar, a Toronto woman with schizophrenia who fatally stabbed a newlywed in a downtown Shoppers Drug Mart in 2015 and was found not criminally responsible in 2018, was granted an absolute discharge by the Ontario Review Board on June 3, 2026, after years of treatment and community-based care; officials say she no longer poses a public-safety threat, but Junor’s family says they hope she stays compliant to keep others safe.
A call-center worker recounts encountering bizarre delusions from customers—phones spying, stalking by corporations, and government radiation claims—and discusses how mental-health issues can shape such calls. The piece offers practical guidance for agents: don’t validate outlandish claims, stay professional, and refocus the conversation on real issues, noting a clever backup method that helped manage these interactions.
A 2023 meta-analysis of 17 studies across 11 countries finds an association between cat exposure and higher risk of schizophrenia-related disorders, with exposed individuals about twice as likely to develop schizophrenia; however, the evidence is observational, often inconsistent, and causality cannot be established, underscoring the need for higher-quality, large-scale research and further exploration of mechanisms like Toxoplasma gondii.
A precision functional genomics study shows the schizophrenia risk gene ZNF804A is most active in glutamatergic neurons during the second trimester. Using CRISPR-Cas9 to suppress ZNF804A in developing neurons increased local protein translation at dendritic tips, raised synapse density, and heightened electrical excitability, linking this genetic risk factor to a specific neurodevelopmental mechanism that may contribute to schizophrenia.
Stanford researchers find neutrophils actively produce C4A, a key schizophrenia risk protein, and in patients these cells pump out more C4A while rapid activation (C4-ana) occurs in plasma. The work links a peripheral immune process to brain synaptic pruning linked to schizophrenia, suggesting blood-based diagnostics and therapies that target the periphery rather than the brain. Clozapine’s neutrophil-depleting effects highlight the need for safer, targeted treatments.
Across seven decades of observations and a major 2018 study, scientists have repeatedly found that people born blind due to cortical (brain) damage do not develop schizophrenia, unlike those who become blind later or whose blindness comes from eye disease. The protection seems tied to how the visual cortex is repurposed early in life, potentially stabilizing the brain’s predictive processing and reducing misfired predictions that underlie psychosis. Timing matters: loss of vision later in life doesn’t confer the same protection. These findings point to new directions for treatment that could target perception, learning, and brain circuits (including glutamate systems in the visual cortex) alongside traditional dopamine-focused approaches, though blindness is not a practical safeguard. This line of research deepens our understanding of brain development and the origins of schizophrenia.”
Kyushu University researchers using super-resolution mapping found that adolescence features a dense hotspot of synapses forming along the apical dendrite of Layer 5 neurons, not just widespread pruning; this selective synapse formation emerges between three and eight weeks in mice and depends on intact synapse-building processes, with mutations in schizophrenia-linked genes Setd1a, Hivep2, and Grin1 impairing hotspot formation. The findings, reported in Science Advances, suggest the pruning-centric view of adolescence is incomplete and future work will identify brain regions where these connections form and whether similar mechanisms occur in humans.
Northwestern researchers found reduced Cacna2d1 protein in schizophrenia; they created a synthetic replacement, SEAD1, and showed that a single injection in mice with a schizophrenia-like genetic duplication normalized brain circuit activity and behavior, with no observed side effects. Human trials are planned but not yet underway.
MIT researchers link a grin2a gene mutation to impaired updating of beliefs in mice via disruption of a mediodorsal thalamus–prefrontal cortex circuit, slowing adaptive decision-making; optogenetic activation of the circuit reversed the behavioral deficits, suggesting circuit-based targets for cognitive symptoms in schizophrenia.
A Johns Hopkins-led study analyzing nearly 700,000 U.S. medical records finds teens with cannabis use disorder have higher risks of schizophrenia, recurrent major depression, and anxiety than peers with other substances, while adults with cannabis use disorder show lower relative psychiatric risk. The researchers propose that cannabis may accelerate onset of mental illness in vulnerable youths or reveal preexisting predispositions, but the results do not prove causation. The findings highlight age-dependent effects and caution against teen use of cannabis, especially high-potency varieties.
The Stanley Family Foundation will donate $280 million to the Broad Institute to advance genetic and genomic research into bipolar disorder and schizophrenia, expanding the Stanley Center’s work and providing stable funding amid uncertain federal support.
Experts say RFK Jr.'s assertion that a ketogenic diet cures schizophrenia is not supported by solid evidence; the only hints come from two 2019 case reports by Harvard psychiatrist Christopher Palmer, which are uncontrolled and cannot establish efficacy. Ketosis may aid symptom remission in some cases, but medical supervision is essential and meds should not be stopped. Around 20 trials are exploring keto for psychiatric conditions, with research into mitochondria and brain activity; long-term adherence and cost pose practical challenges, so no cure is proven yet.
Kennedy’s claim that ketogenic diets cure schizophrenia is not supported by current science. Evidence is preliminary, coming from small studies and case reports that suggest possible symptom improvement when ketosis is achieved under medical supervision, but large, randomized trials showing clear benefit over medication alone are lacking. The Stanford study reported most adherent patients improved but had no control group, and researchers caution that keto should supplement rather than replace antipsychotic treatment while more rigorous research is underway.