Recent findings are reshaping current understanding of the post-infection landscape of SARS-CoV-2. Although previous studies had already suggested that autoimmunity might underlie the persistent neurological symptoms seen in long COVID, researchers at Yale University and Mount Sinai now reinforce this hypothesis. SARS-CoV-2 infection appears to trigger an autoimmune mechanism that drives chronic pain, fatigue and cognitive impairment in some patients.
Andzonbio2 has signed agreements with the Alborada Drug Discovery Institute (ADDI) at the University of Cambridge and Cambridge Enterprise to advance a new class of therapeutics targeting neuroinflammation, a central driver of multiple neurodegenerative and neurological conditions.
Chinese researchers have published data regarding phosphatidylserine (PS) derivatives acting as neuroprotective compounds for Alzheimer’s disease (AD) therapy.
Parkinson’s disease is a progressive neurodegenerative disorder best known for its motor symptoms. However, a proportion of patients also develop dementia as the condition advances. Yet the biological divide between those who experience this cognitive decline and those who do not has remained an open question. Are they different conditions or simply stages of the same disease?
Microglia play a central role in the neuroinflammation associated with Alzheimer’s disease (AD). 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.
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.
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.
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.
Vandria SA published phase I data on a potential new mechanism of action in treating Alzheimer’s disease, demonstrating its orally available and brain-penetrant mitochondria-boosting compound, VNA-318, engages its intended target.
