Microglia is known to play a crucial role in brain homeostasis, but this is lost during neurodegeneration.

Galectin-3 (Gal-3) is used as a marker of activated microglia, and thus a protein that drives inflammation. Patients with Alzheimer’s disease (AD) have shown increased levels of Gal-3 in their cerebrospinal fluid (CSF) compared to healthy controls, as well as increased expression in their brain tissue.

After many years of testing different monoclonal antibodies against amyloid-β protein, the results obtained are far from being outstanding, and the control of the progression and symptoms of Alzheimer’s disease (AD) remains elusive. At the recent AD/PD 2024 conference held in Lisbon, new non-anti-amyloidogenic strategies in the starting line against AD were discussed. Professor Einar Sigurdsson from New York University gave a presentation entitled, “Single domain antibodies for therapy and diagnosis of synucleinopathies and tauopathies.”

Researchers from Massachusetts General Hospital recently detailed the discovery of [11C]SY-08, a new PET radiotracer that detects aggregated α-synuclein (α-Syn) fibrils in individuals with neurological disorders such as Parkinson’s disease, multiple system atrophy and dementia with Lewy bodies.

After many years of testing different monoclonal antibodies against amyloid-β protein, the results obtained are far from being outstanding, and the control of the progression and symptoms of Alzheimer’s disease (AD) remains elusive. At the recent AD/PD 2024 conference held in Lisbon, new non-anti-amyloidogenic strategies in the starting line against AD were discussed. Professor Einar Sigurdsson from New York University gave a presentation entitled, “Single domain antibodies for therapy and diagnosis of synucleinopathies and tauopathies.”

Prosetta Biosciences Inc. has presented data on small molecules that inhibit cellular host factors needed for viral replication as a discovery tool to identify molecular interfaces upstream of Alzheimer’s disease cellular pathology.

It has been previously demonstrated that genetic loss-of-function of triggering receptor expressed on myeloid cells 2 (TREM2) impairs microglia migration, with the TREM2 R47H variant having been linked to increased risk of Alzheimer’s disease (AD) due to impaired microglia clustering and enhanced neuronal damage.

Recent studies have identified HAVCR2, which encodes immune checkpoint molecule TIM-3 (T-cell immunoglobulin mucin receptor 3), as a risk gene for late-onset Alzheimer’s disease (AD).

Deep molecular profiling of cell types in the brain is needed to uncover the mechanisms behind neurodegeneration.