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CervoMed Announces New Data at the AD/PD™ 2026 Scientific Conference that Reinforce Neflamapimod’s Positive Effects in Dementia with Lewy Bodies (DLB) in Patients without Alzheimer’s Disease Co-Pathology
New analyses show DLB patients with lower plasma pTau181 levels — indicating an earlier stage of disease and absence of Alzheimer’s disease (AD) co-pathology
About this update from Cervomed Inc.
[{"type":"text","content":"New analyses show DLB patients with lower plasma pTau181 levels — indicating an earlier stage of disease and absence of Alzheimer’s disease (AD) co-pathology — experienced greater clinical benefit with neflamapimod in Phase 2b clinical trial PK/PD analyses of Phase 2b clinical data provide further insight into the drug plasma concentration levels of neflamapimod associated with a clinical effect Findings further support neflamapimod’s potential to target the underlying cause of disease in DLB and the Company’s patient enrichment strategy and dosing regimen for planned Phase 3 trial BOSTON, March 19, 2026 (GLOBE NEWSWIRE) -- This week, in an oral session at the AD/PD™ 2026 Conference in Copenhagen, Denmark, investigators will present new analyses from the Phase 2b RewinD-LB clinical trial of neflamapimod, being developed by CervoMed Inc. (NASDAQ: CRVO) (CervoMed or the Company) for the treatment of dementia with Lewy bodies (DLB). The new data analyses reinforce that neflamapimod, which targets the neuroinflammation and synaptic dysfunction associated with DLB, has the potential to slow disease progression by acting on the underlying disease biology. “In these analyses, the treatment response progressively increases across DLB patient subgroups that are less likely to have Alzheimer’s disease (AD) co-pathology, as identified by the pTau181 blood test,” said Dr. John-Paul Taylor, MBBS, MRCPsych, PhD, Professor of Translational Dementia Research at Newcastle University and the chief investigator of the RewinD-LB trial for the United Kingdom. “These data further validate the use of plasma pTau181 to exclude patients with AD co-pathology, potentially enabling us to focus on those most likely to experience a treatment benefit with neflamapimod. In addition, because neflamapimod targets the biology driving ‘pure’ DLB, the robust association between neflamapimod response and absence of AD co-pathology strengthens our confidence that neflamapimod can slow disease progression in these patients.” “The clinical and biomarker activity that we are seeing with neflamapimod provides a strong indication that we are successfully targeting the underlying cause of disease in the basal forebrain and supports our belief that the inhibition of p38α by neflamapimod can reverse the synaptic dysfunction that drives disease progression in ’pure‘ DLB patie...