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.
Medullary thyroid carcinoma (MTC) is a rare, often aggressive, neuroendocrine thyroid tumor with limited targeted treatment options, arising from calcitonin-producing C cells and sometimes associated with RET mutations. Researchers from the Mayo Clinic reported the potential of targeting DLL3 as a therapeutic strategy in MTC.
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.
Researchers from Incyte Corp. reported the efficacy of INCB-161734, a KRAS G12D inhibitor, in combination with various strategies in models of pancreatic ductal adenocarcinomas (PDACs).
At the ESMO Targeted Anticancer Therapies Congress held this week in Paris, researchers at Mabqi SAS presented the preclinical characterization of MQI-201, an anti-TRPV6 therapeutic antibody in models of metastatic prostate cancer.
At the ongoing International Conference on Alzheimer’s and Parkinson’s Diseases and Related Neurological Disorders (AD/PD 2026) in Copenhagen, researchers presented details on a new SERCA inhibitor from Synuca Therapeutics ApS – SYN-4569 – as a potential approach to treat multiple system atrophy-cerebellar type (MSA-C).
A new way of understanding Alzheimer’s disease, based on biological inflection points that mark decisive moments in the progression of the disorder, could change how new drugs are developed to achieve more effective therapies. This new perspective could rethink strategies that depend not so much on the target itself, but on the precise moment at which it is addressed.
Exon skipping therapies based on antisense phosphorodiamidate morpholino oligomer (PMO) have great potential to restore dystrophin in the skeletal muscle and treat Duchenne muscular dystrophy (DMD). Entrada Therapeutics Inc. has developed an endosomal escape vehicle conjugated to DMD exon skipping PMOs (exon 51 skipping), ENTR-601-51, for the potential treatment of DMD.
Neurodegenerative disease and cognitive decline cannot be explained by a single process. Beta-amyloid plaques, hyperphosphorylated tau, alpha-synuclein, activated microglia and astrocytes, altered receptors such as TREM2, mitochondrial dysfunction, epigenetic changes and cerebrovascular alterations all seem to contribute to the development of dementia in Alzheimer’s disease (AD). While scientists attempt to address each of these elements, prevention is growing as a primary goal.
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