Sichuan Primed Shines Bio-Tech Co. Ltd. researchers have published results on their investigation regarding SYW-06 oral dosing and its impact on cognitive function in monkeys submitted to middle-cerebral artery occlusion (MCAO).
The potent carboxypeptidase enzyme protective protein cathepsin A (PPCA) is known to cleave the C-terminus of amyloid-β42, responsible for aggregation and oligomer stability, and may reduce both intracellular and extracellular amyloid-β aggregates in the brain. Amlogenyx Inc. has presented data regarding their approach based on PPCA delivery through an adenoviral vector (AAV9), namely AM-805, for the potential treatment of Alzheimer’s disease (AD).
Microglia play a central role in the neuroinflammation associated with Alzheimer’s disease (AD). These cells act as the brain’s immune system and respond to damage signals such as amyloid accumulation. When the process starts, the initial microglial response can be protective. However, in later stages, this response becomes dysfunctional and contributes to disease progression. At the 20th International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD), scientists focused on TREM2, a microglial receptor that regulates immune responses, exploring new ways to address neuroinflammation.
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.
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.
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.
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