Latest Alzheimer Disease Data: Reports from CTAD 2025

Trontinemab Shows Promise for Treatment of Alzheimer Disease in New Data at CTAD

Trontinemab showed a 92% reduction in amyloid plaques, according to new data from the Brainshuttle AD trial. The drug showed an ability to lower amyloid levels and even potentially affect tau accumulation, while minimizing brain swelling or bleeding commonly seen. Further studies on trontinemab are planned, and the current Brainshuttle AD study anticipates primary completion in mid 2030. Read more here.

Data Fails to Show Significant Change in Cognition and Function With Oral Semaglutide for Early Alzheimer Disease

With highly anticipated results, oral semaglutide unfortunately failed to show significant improvement in cognition or function in participants with early Alzheimer disease. In the Evoke and Evoke+ trials, older adults in a 2-year study taking oral semaglutide did not show slowed cognitive or functional decline compared with placebo. Trial developers noted that these results are disappointing but still provide useful information in the Alzheimer disease research space. Read the news here.

Favorable Profile Data On MK-2214 for Treatment of Alzheimer Disease

Data on MK-2214 showed favorable profile in treating Alzheimer disease, addressing tau accumulation in particular. The phase 1 trial of this drug demonstrated acceptable tolerability at all dose levels used, with no dose-limiting tolerability issues or serious drug-related adverse events. MK-2214 has been granted Fast Track designation by the US Food and Drug Administration and will continue with the ongoing phase 2 trial. See more here.

Data Presentation on XPro1595 for Alzheimer Disease With Inflammation at CTAD

Positive new data was shared from the phase 2 MINDFuL trial of XPro1595 for early Alzheimer disease and neuroinflammation. Data presentation showed slowed disease progression, thought to indicate fighting disarray in the cortical structure. Using PerpPD+, an MRI analysis, the study highlighted lessened structural issues with XPro1595 and a consequent slowing of neurodegeneration. Read more here.