Immunotherapy is a rapidly evolving field in pediatric neuro-oncology, using diverse strategies to enhance or initiate an antitumor immune response. Its use has expanded from hematologic malignancies to solid central nervous system (CNS) tumors, creating new diagnostic challenges in neuroimaging, particularly in children.

The aim of this review is to summarize current immunotherapeutic strategies for pediatric solid CNS tumors and to discuss their characteristic imaging findings and response patterns, with emphasis on pitfalls in differentiating true progression from treatment‑related inflammatory changes.

Across different immunotherapeutic approaches, a major challenge is distinguishing tumor progression from pseudoprogression, immune‑related flare phenomena, and neurotoxicity. Multiparametric imaging combining advanced MRI techniques and metabolic imaging may improve diagnostic specificity; however, validation in children is limited, and existing response frameworks such as iRANO and RAPNO do not specifically address immunotherapy‑related imaging patterns in the pediatric population.

A blood test for the biomarker phosphorylated tau 217 (p-tau217) recently received federal clearance, but questions have emerged about the extent to which such tests can accurately predict whether a cognitively healthy individual will develop cognitive impairment—a key symptom of Alzheimer’s disease.

A new international study involving researchers across three continents and led by experts from the Mass General Brigham Neuroscience Institute sheds new light on the prognostic value of such tests.

The study found that cognitively unimpaired individuals with very high levels of the biomarker had a 38% absolute risk of developing cognitive impairment over the next five years and a 78% risk over the next 10 years.

A newly discovered signaling network transmits advanced intelligence from distal regions of the body to the blood-brain barrier, giving the brain time to ready itself.

It turns out that tau is not just Alzheimer’s foe, as new study finds it also builds lasting memories.

An analysis of the brain of a deceased Alzheimer’s disease (AD) clinical trial participant found that regions where an anti-amyloid therapy successfully cleared amyloid plaques showed little to no evidence of tau tangles, a hallmark of AD closely linked to neurodegeneration and cognitive decline. In contrast, neighboring areas where amyloid remained showed substantially more tau pathology and signs of ongoing brain damage.

The findings provide rare human evidence that clearing amyloid plaques may have long-term effects on the biological processes that drive AD. The study also suggests that removing amyloid early and extensively may slow the progression of the disease by limiting the accumulation of tau and subsequent neurodegeneration, according to findings presented July 13 at the 2026 Alzheimer’s Association International Conference by researchers from the Perelman School of Medicine at the University of Pennsylvania. The report was also concurrently published in JAMA.

“Seeing both disease patterns side-by-side in the same brain gave us a rare opportunity to understand how amyloid removal affects other proteins that contribute to Alzheimer’s disease,” said co-senior author David Wolk, MD, co-director of the Penn Memory Center and director of the Penn Alzheimer’s Disease Research Center. “The findings provide some of the clearest human evidence to date that anti-amyloid therapies may limit the accumulation of tau and slow the brain changes that lead to memory loss and cognitive decline.”