To overcome the limitations regarding conventional immunotherapy for treating tauopathies, researchers from Sanofi SA aimed to improve brain exposure and targeting pathological tau species by optimizing antibody design.
Gene editing holds promise for treating neuromuscular disorders such as limb-girdle muscular dystrophy, but its clinical translation remains challenging due to a lack of complementary delivery tools for the extensive network of skeletal muscles in the human body. A team at University of Massachusetts Chan Medical School compared editing outcomes mediated by either Cas9 mRNA and RNP delivery to skeletal muscle via local injection in the context of the previously described selective organ targeting (SORT) lipid nanoparticles (LNPs) platform.
Discoveric Bio Alpha Ltd. and collaborators have presented data regarding the rationale and design of NIDB-3101, a third-generation, human IgG1 anti-tau biparatopic antibody for the treatment of Alzheimer’s disease (AD).
Soluble amyloid-β oligomers (AβOs) are known early drivers of Alzheimer’s disease pathogenesis. Acumen Pharmaceuticals Inc. has recently presented data generated in the development and characterization of anti-AβO antibodies with high selectivity for AβO over Aβ monomers.
Insitro Inc. has expanded its strategic collaboration with Bristol Myers Squibb Co. to advance a broadened portfolio of therapeutic programs for amyotrophic lateral sclerosis (ALS).
Neuroinflammation has arisen as a key factor in the pathophysiology of Alzheimer’s disease (AD). Chronic immune activation in the brain leads to the release of pro-inflammatory cytokines and other inflammatory mediators that contribute to neuronal damage, thus impacting cognitive function during the progression of the disease. Transcriptomic and epigenomic analyses were performed to understand the epigenetic mechanisms behind the expression of inflammatory genes in AD brain.
Researchers from Arthex Biotech SL, the University of Valencia (Spain) and collaborators sought to address the lack of optimized microRNA (miRNA)-targeting antisense oligonucleotides (anti-miRs) for upregulating MBNL1 in myotonic dystrophy.
A new Danish research project focused on Parkinson’s disease has received funding from Innovation Fund Denmark. The DESYNA (Degradation of Extracellular α-SYNuclein Aggregates) project aims to develop a new therapy targeting α-synuclein, the accumulation of which is a key driver of Parkinson’s disease.
The aberrant activation of NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is a known crucial driver of neuroinflammation in Alzheimer’s disease (AD) and other related dementias. The inhibition of NLRP3 has shown benefits in preclinical models. Researchers from the University of Texas recently presented data regarding an NLRP3 inhibitor, AMS-17, for the treatment of AD and related dementias.
Parkinson’s disease (PD) involves the progressive loss of dopaminergic neurons, particularly in the substantia nigra. This neurodegeneration is linked to the abnormal accumulation of α-synuclein, a protein that forms toxic aggregates and spreads between cells, damaging them. At the 20th International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD), held from March 17 to 21, 2026, in Copenhagen, several strategies were presented that aim to modify the course of the disease and offer real alternatives to purely symptomatic treatments.
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