Kv1.3 is a voltage-gated potassium channel that plays a crucial role in neuroinflammation and neurodegeneration in Parkinson’s disease and other disorders. Preclinical studies have shown that Kv1.3 inhibition confers neuroprotection against neurodegenerative disorders.
Alterations in mitochondrial dynamics are hallmarks of Parkinson’s disease (PD) and other neurodegenerative disorders such as Alzheimer’s disease (AD).
Advances in understanding the processes underlying brain neurodegeneration have allowed lots of new treatment and prevention strategies to begin to flourish. Several presentations at the 2024 Alzheimer’s & Parkinson’s Diseases Conference recently held in Lisbon reflect that eyes are now on some individuals who, despite showing pathological signs in their brains, stay cognitively healthy across several endogenous mechanisms of resilience.
In a new study, researchers from Harvard Medical School and Regulus Therapeutics Inc. further investigated the role of miR-155 in Alzheimer's disease (AD).
The activation of the NLRP3 inflammasome exacerbates neuronal dysfunction in several neurological diseases such as Alzheimer’s and Parkinson’s diseases, as well as multiple sclerosis. Targeting NLRP3 is an approach to overcome brain inflammation, among others.
The small-molecule steroid sulfatase (STS) inhibitor STX-64 (ONESTX-1, irosustat) previously showed a good safety and tolerability profile in several phase I and II clinical trials that evaluated the candidate for oncology indications.
Recent findings have suggested GAL-201 from Galimedix Therapeutics Inc. is a robust oral candidate to treat Alzheimer’s disease (AD). GAL-201 binds to the misfolded form of amyloid-β (Aβ) monomers, thus preventing its aggregation and formation of neurotoxic oligomers and protofibrils.
The third day of the AD/PD 2024 conference in Lisbon started with a plenary lecture given by Professor Howard Fillit entitled, “Translating the biology of aging into new therapeutics for Alzheimer’s disease.” Fillit, a recognized neuroscientist and geriatrician, and co-founder of the Alzheimer’s Drug Discovery Foundation (ADDF), pointed to the geroscience hypothesis which postulates that targeting aging processes may result in preventive and therapeutic options for diseases of old age, including Alzheimer’s disease (AD).
It has been previously demonstrated that TREM2 is extensively shed during chronic neuroinflammation, which hiders its function, while TREM2 activation enhances effector functions of microglia.