Video Series

Realizing functional cure at scale will take more than new drugs; it requires infrastructure, testing, and patient engagement working in concert. This episode closes the series with a roadmap for that shift.

Will vitiligo treatment settle into a clear sequencing algorithm, or remain individualized? Dr. Lal and Jason weigh the absence of clinical guidelines against the reality that professional consensus typically lags well behind new therapies.

Concurrent chemoradiotherapy remains curative-intent therapy for limited-stage disease, yet cure rates without immunotherapy stall near thirty percent, a ceiling that scheduling choices and careful monitoring can only partly raise on their own.

A serum level is a snapshot, while genotype is the blueprint. Relying on levels alone misses carriers and mislabels patients, and the resulting diagnostic gap carries real clinical and economic costs.

AATD is better understood as a genetic predisposition than a single disease. Genotype, codominant inheritance, and environmental exposure together shape who develops lung or liver disease and how severe it becomes.

Before comparing therapies, clinicians need the statistical vocabulary: what a p-value actually measures, why effect size matters more, and how network meta-analysis links trials through a shared placebo comparison.

Small cell lung cancer's stark divide between curable, localized disease and systemic, incurable disease shapes every treatment decision that follows, and screening gains are slowly shifting how many patients get caught early enough to benefit.

Led by the moderator, the expert neurology and primary care panelists examined the gap between expanded coverage and real-world access.

Led by the moderator, the panelists discussed how they sequence plasma p-tau217 and beta-amyloid 42/40 testing alongside cognitive screening as a first-line workup, reserving confirmatory amyloid PET or CSF testing for inconclusive cases, and noted that payer coverage for these biomarker tests has so far been largely free of denials.

With three oral JAK inhibitors advancing through Phase 3 trials, Dr. Rosmarin calls for consensus guidelines, while Dr. Desai details the practical advocacy, documentation, and coverage groundwork needed to get patients access.

Early signals from a TLR9 agonist point to a role for innate immune modulation, though likely as one piece of a larger combination strategy rather than a standalone cure. This episode explains why.

As treatment options multiply, Jason and Dr. Lal weigh localized versus systemic delivery against body surface area, safety, and real-world absorption risk, questioning whether cost alone should keep topical therapy as the default choice.

With no head-to-head trials among the five adjunctive antipsychotics approved for major depressive disorder, payers default to skepticism toward branded options unless indirect comparative evidence proves added value beyond cost.

The panelists examined the hurdles of practicing without local backup.

From host-directed therapies to inhaled drug delivery, Dr. Losier maps the research priorities that could finally match the right MAC and NTM treatment to the right patient.

Led by the moderator, the expert neurology and primary care panelists examined what an ideal training curriculum looks like.

Led by the moderator, the panelists/expert mental health experts examined key patient-level factors driving selection among the five adjunctive agents — including weight status, sleep disturbance, and general medication sensitivity — with Wilkinson noting a preference for lumateperone given its lack of weight gain and quetiapine for patients needing help with sedation who aren't already overweight, while Bhide observed these are exactly the clinical factors payers would want documented under utilization management.

Led by the moderator, the expert mental health experts examined network meta-analysis data comparing weight gain and akathisia across the five agents, with Rhee noting lumateperone did not differ from placebo on weight gain while the other four agents showed increased risk, and cautioning that these exploratory findings warrant careful interpretation given limited clinical data.

A newer generation of capsid assembly modulators may finally move the needle on surface antigen, something earlier compounds in this class could not achieve. This episode explores that shift.

Black box warnings drawn from a distinct, higher-risk population have colored perceptions of JAK inhibitor safety in vitiligo. Dr. Desai argues for contextualized risk communication, appropriate screening, and recognizing genuine comorbidity benefits.

A roughly 20% functional cure rate is meaningful, but it comes with a safety profile that demands scrutiny in patients already doing well on suppressive therapy. This episode weighs that tradeoff.

Two years of ruxolitinib cream data show continued gains rather than a plateau, and Dr. Rosmarin argues that early initiation prevents a repigmentation gap patients never fully close. Jason explains why payers remain cautious regardless.

Led by the moderator, the panelists discussed how lecanemab and donanemab differ in trial efficacy, dosing schedule, and administration route, and how ARIA — while it can sound alarming to patients — is usually asymptomatic and stratifiable by a patient's APOE4 status, requiring the most intensive MRI monitoring in the first six months of treatment before rates drop off.

Culture conversion alone cannot capture what patients experience during MAC treatment, and new patient-reported outcome data argue for a more multidimensional definition of treatment success.

Early data on inhaled clofazimine suggest the drug can reach the lung at meaningful concentrations with far less systemic exposure than oral therapy, though efficacy evidence remains preliminary.

The panelists examined the full treatment continuum for Alzheimer's disease.

Led by the moderator, the panelists discussed brexpiprazole's pivotal two-phase trial design and how its reduced intrinsic dopamine partial agonism and lower starting doses contributed to fewer akathisia events than aripiprazole, followed by cariprazine's D3-preferring mechanism and more favorable metabolic and sedation profile.

The panelists examined aripiprazole's pivotal trial design, which used an antidepressant lead-in phase followed by randomization to placebo or active drug among non-responders, with Thase detailing how dose-finding evolved toward lower 5 mg and 10 mg doses to minimize akathisia, the primary dose-limiting side effect, while preserving antidepressant benefit at doses lower than those used for antipsychotic indications.