Kinase inhibitors have shown success in disease areas such as oncology, but their application in neurodegenerative diseases is still limited. This is mainly due to several challenges, such as the complexity of kinase networks, limited blood-brain barrier permeability and the lack of biomarkers.

Just over a month after emerging from stealth and disclosing a $150 million series A, Korsana Biosciences Inc. is making the leap to the public market via a merger with Cyclerion Therapeutics Inc.  The agreement, which is backed by a $370 million private placement from Korsana’s investors, solidly positions the newly merged company as it heads toward the clinic with KRSA-028, a next-generation shuttled antibody targeting amyloid beta for the treatment of Alzheimer’s disease, and builds out a pipeline of neurodegenerative disease candidates.

Just over a month after emerging from stealth and disclosing a $150 million series A, Korsana Biosciences Inc. is making the leap to the public market via a merger with Cyclerion Therapeutics Inc.  The agreement, which is backed by a $370 million private placement from Korsana’s investors, solidly positions the newly merged company as it heads toward the clinic with KRSA-028, a next-generation shuttled antibody targeting amyloid beta for the treatment of Alzheimer’s disease, and builds out a pipeline of neurodegenerative disease candidates.

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. 

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).

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.