Researchers at ETH Zurich have identified a proteomic signature that could recognize long COVID six months after acute infection. Biologically, the signature indicated that the complement system remained active in patients with long COVID six months after infection. Translationally, it could lead to a diagnostic test for long COVID, and suggests that targeting the complement system could be a therapeutic approach to prevent or treat the disorder.
Alzheimer’s disease (AD) can be divided into five distinct subtypes based on protein expression levels measured in the cerebrospinal fluid (CSF). The subtypes were associated with different genetic risk factors and are likely to benefit from different treatment approaches.
Many clinicians, drug developers and the general public still “think of Alzheimer’s as a single disease entity, and that suggests that every patient needs to have the same medication,” Betty Tijms told BioWorld.
If we unraveled the DNA of the 46 chromosomes of a single human cell, it would barely measure 2 meters. If we did the same with the rest of the body, if we aligned the 3 billion base pairs of its 5 trillion cells, we could travel the distance from the Earth to the Sun more than 100 times. It seems unreachable. However, that is the unit of knowledge of the large sequencing projects achieved in 2023. From the generation of the human pangenome to cell-by-cell maps of the brain and kidneys, scientists this year have completed several omics collaborative projects stored in large international databases. Now, what’s the plan?
The broadest view of post-mortem brains in Alzheimer’s disease (AD) has unveiled the genome, transcriptome and epigenome alterations of this neurodegenerative condition. The coordinated research, directed by scientists at the Massachusetts Institute of Technology (MIT), also described new cellular pathways that could help the scientific community design new therapies. Four simultaneous studies published on Sept. 28, 2023, in Cell, presented a brain single-cell atlas of AD, exposed the damage that affects DNA, and described the processes that alter the microglia and dysregulate the epigenome.
The vast variety of tumors makes each cancer a world. For researchers, understanding the commonalities and divergences in their molecular underpinnings could help find successful treatments. Scientists from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) have addressed these similarities and differences in 10 different types of cancer with two proteogenomic studies to unravel the genes that lead to cancer and the galaxy of interactions that regulate them.
The degradation pathways of cellular components can be shared by different molecules or selectively replace different substances and organelles. In the brain, synaptic transmission involves signaling pathways for a wide range of molecules, vesicles and receptors that require constant recycling. A proteomic study from the University of Lausanne and the University of Fribourg sheds light on brain autophagy-selective routes in adolescent, adult and aged brains.
The map of the genetic activity of the risk genes that affect the central nervous system (CNS) reveals the molecular signatures associated with the neurological pathologies in this organ. A study by researchers at McGill University in Canada and the Allen Institute for Brain Science in Washington compared 40 brain diseases with this technology and classified them into five groups whose members shared the same transcriptional pattern.
Researchers have gained new insights into physiological mechanisms that protect against blood clotting in immobilized individuals by studying animals that stay immobile for a good chunk of the year at a time: hibernating bears. “As a clinician, if you think about immobility, you always think about thrombosis,” Tobias Petzold told BioWorld. But his team’s work, which was published in the April 13, 2023, issue of Science, demonstrated that “immobility can trigger antithrombotic mechanisms.”
The analysis of thousands of proteins in the brain has revealed the association of astrocytes with obsessive-compulsive disorder (OCD). A proteomic study by researchers from the University of California Los Angeles (UCLA) has identified them in different cellular compartments of astrocytes and neurons. One such protein, the postsynaptic protein SAPAP3, appeared to regulate the organization of the actin cytoskeleton. Its deficit in astrocytes could cause OCD.
RNA editing in schizophrenia (SCZ)-associated genes was decreased in postmortem brains of individuals of European descent, according to a study from the University of California, Los Angeles (UCLA). The scientists obtained the RNA editome from SCZ brains to detect the sequence changes in their RNA and observed hypoediting in noncoding regions related to mitochondrial function, such as the mitofusin-1 (MFN1) gene.