The difference between the origin of Alzheimer's disease (AD) and its symptoms is an obstacle to finding effective treatments. Scientists focused on amyloid-β (Aβ) plaques and tau aggregates to slow neurodegeneration and cognitive decline. Without identifying what causes AD, approved treatments do not provide much benefit. However, new findings suggest that restoring lithium levels in the brain could prevent and treat AD. Not just any lithium would work, just the forms that do not bind to Aβ.

Abnormal tau aggregation is a hallmark of Alzheimer’s disease (AD) and a major contributor to neurodegeneration, synaptic dysfunction, and progressive functional decline. Antibodies against extracellular tau represent a potential therapeutic approach aimed at reducing pathological spread and delaying the clinical progression of AD. Researchers from Merck & Co., Inc. presented the preclinical development of MK-2214, a murine IgG2a monoclonal antibody that selectively targets the pathological phospho-epitope pSer413 of the tau protein.

Lysoway Therapeutics Inc. announced that it has received a research grant of $2.93 million from The Michael J. Fox Foundation for Parkinson's Research. The funding will support the preclinical development of Lysoway’s highly brain-penetrant small molecule mucolipin TRP Cation channel 1 (MCOLN1/TRPML1) agonist.

In the tumor microenvironment, cancer cells activate various signaling pathways to promote their growth. This includes the formation of blood vessels. However, the circulatory system is not the only one attracted to the tumor. Researchers at Sanford Research have uncovered a mechanism to circumvent the immune response that would destroy them.

At the Alzheimer's Association International Conference (AAIC) 2025, researchers from Acadia Pharmaceuticals Inc. have presented novel results on the assessment of the pharmacologic and pharmacokinetic (PK) properties and nonclinical safety of ACP-204.

In Alzheimer’s disease (AD), degeneration of synapses, including synaptic spines, has been linked to cognitive losses.

Subtyping is what made precision medicine in cancer a reality. And for successful drug discovery in all its stages, finding subtypes in Alzheimer’s disease is all but imperative. Prior to the approval of the modestly effective Lequembi (lecanemab, Biogen Inc./Eisai Co. Ltd.) Kisunla (donanemab, Eli Lilly and Co.), and the since-withdrawn Aduhelm (aducanumab, Biogen Inc./Eisai Co. Ltd.), more than a dozen failed phase III clinical trials were all that amyloid-targeting drugs had to show for themselves for decades of effort.

Researchers from Suven Life Sciences Ltd. have presented results on the evaluation of the pharmacological properties of SUVN-I6107 in various animal models of cognitive deficits at the Alzheimer's Association International Conference (AAIC) 2025.