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Blood and spinal fluid proteins reveal distinct fingerprints of four brain diseases

Researchers at WashU Medicine have uncovered new molecular insights into Alzheimer’s disease, Parkinson’s disease and other forms of dementia by analyzing thousands of proteins in both cerebrospinal fluid and blood plasma. The study, led by Carlos Cruchaga, the Barbara Burton & Reuben Morriss III Professor in the Department of Psychiatry and director of the NeuroGenomics and Informatics Center at WashU Medicine, represents one of the largest and most comprehensive multi-tissue analyses of proteins across multiple neurodegenerative diseases to date. The findings raise the possibility of developing blood tests for earlier and more precise diagnosis of these conditions.

In the study, published March 30 in Neuron, a multi-institutional team of clinicians, neuroscientists and data scientists, steered by Muhammad Ali, an assistant professor of psychiatry at WashU Medicine and first author of the study, analyzed nearly 7,000 proteins in samples of spinal fluid and blood from nearly 6,000 people—including people with neurodegenerative diseases as well as healthy controls—to better understand four major neurodegenerative diseases: Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, and frontotemporal dementia.

By analyzing these diseases in parallel, the researchers could distinguish both shared and disease‑specific “molecular fingerprints.” Across all four diseases, the protein analysis indicated clear evidence of inflammation, damage to the connections between nerve cells, and changes in the scaffolding around cells known as the extracellular matrix.

Chromosomes condense in three timed chemical waves during cell division, study shows

DNA does not float freely in the cell. Instead, it is wrapped around histone proteins to form structures called nucleosomes. These histones carry numerous chemical modifications that act as molecular signals, controlling how tightly the DNA is packaged and which genes are active. During cell division, this DNA-histone complex—known as chromatin—must be further condensed into compact, rod-shaped chromosomes. Histone modifications play a key role in this process: They change significantly during condensation and regulate the conversion of chromatin.

For the first time, researchers have precisely tracked how molecular marks on DNA proteins change during cell division—and disproved a long-held assumption in the process.

An international research team led by Professor Axel Imhof at LMU’s Biomedical Center and Professor William Earnshaw (University of Edinburgh) has analyzed these changes during cell division with unprecedented precision. To this end, the researchers developed an innovative method that synchronizes the division of cell populations. They then employed high-resolution mass spectrometry to precisely record the changes in histone modifications during cell division. The findings are published in Molecular Cell.

The Immune System Impacts Longevity: What To Measure

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Boosting good gut bacteria population through targeted interventions may slow cognitive decline

The origin of neurodegenerative diseases like Alzheimer’s or dementia isn’t limited to the brain. The state of your gut can quietly set off a cycle of chronic, system-wide inflammation that nudges the brain toward cognitive decline. But how does the pathogenesis of a disease that seems purely brain-based begin in the gut—an organ that is mostly busy producing chemicals for digesting food?

It turns out these two entities are linked by the gut-brain axis, a two-way communication superhighway that constantly sends signals between the digestive tract and the central nervous system. It runs on chemical messengers like neurotransmitters and fatty acids, sharing information that shapes our memory, mood, and inflammation triggers.

An analysis of 15 studies involving more than 4,200 participants found that the gut-brain highway can be put to work as a drug-free route to support cognitive health. Tuning the gut microbiota through diet, supplements, or medical interventions such as fecal microbiota transplantation (FMT) can help improve memory, executive function, and overall cognitive performance, particularly in early or mild cases of cognitive impairment.

Phage therapy case reveals hidden antibodies can block treatment of drug-resistant infections

A new treatment for patients with life-threatening infectious diseases is being pioneered in Melbourne by researchers at The Alfred and Monash University. VICPhage, a clinical partnership between The Alfred and Monash, is one of the first in Australia to offer end-to-end capacity in phage therapy to treat some of the most challenging infections.

It involves injecting a patient with viruses called bacteriophages, or phages for short, to kill bacterial infections that have not responded to other treatments.

Professor Anton Peleg, Director of the Department of Infectious Diseases at The Alfred and Monash University and the Center to Impact AMR at Monash University, is co-lead of VICPhage and senior author of a new paper published in Nature Medicine.

How parasites exit host cells

After infecting host cells and reproducing, the parasite life cycle requires them to egress so that they can move to the next host. Past studies on the genes required for this process have been conducted but show conflicting results.

The methodology of past studies often involved opening the host cells during the screening process. Consequently, researchers were unable to reliably identify when mutations prevent parasites from egressing.

To avoid the same limitations, the team used an in vivo approach to screen for essential genes instead.

“Our in vivo screen, based on CRISPR, identified for the first time that the MIC11 gene is essential for host cell membrane permeabilization and parasite egress.” Explains the lead author.

Further tests demonstrated that deleting the MIC11 gene led the parasites to be unable to rupture the host cell membrane. By incapacitating parasites in this way, they could no longer exit the host cells, majorly disrupting the parasite life cycle.

“We also found evidence that MIC11 interacts with PLP1, providing further evidence of MIC11’s crucial role,” explains the senior author. “PLP1 is another parasite protein that was already known to be essential for egress.” ScienceMission sciencenewshighlights.

Continue reading “How parasites exit host cells” | >

Frontiers: Year 2020 this gene therapy in mice shows promise for als gene therapy in humans

Gene therapy is an emerging and powerful therapeutic tool to deliver functional genetic material to cells in order to correct a defective gene. During the past decades, several studies have demonstrated the potential of AAV-based gene therapies for the treatment of neurodegenerative diseases. While some clinical studies have failed to demonstrate therapeutic efficacy, the use of AAV as a delivery tool has demonstrated to be safe. Here, we discuss the past, current and future perspectives of gene therapies for neurodegenerative diseases. We also discuss the current advances on the newly emerging RNAi-based gene therapies which has been widely studied in preclinical model and recently also made it to the clinic.

Gene therapy is an emerging therapeutic tool used to deliver functional genetic material to cells in order to correct a defective gene. By delivering a copy of a therapeutic gene to affected cells, the product encoded by that gene [i.e., its messenger RNA (mRNA) and/or proteins] will be continuously synthesized within the cell, utilizing the cell’s own transcriptional and translational machinery (Porada et al., 2013). The main advantage of this technology is that it offers a potentially life-long therapeutic effect without the need for repeated administration. Gene therapy can be used to correct defective genes by introducing a functional copy of the gene, by silencing a mutant allele using RNA interference (RNAi), by introducing a disease-modifying gene, or by using gene-editing technology (Grimm and Kay, 2007; Dow et al., 2015; Saraiva et al., 2016).

Gene therapy vectors can be either viral or non-viral. Different physical and chemical systems can be applied to deliver therapeutic genes to cells without the need of a viral vector. Non-viral vectors have no size limitation for the therapeutic gene, generally have a low immunogenicity risk, and can be produced at relatively low costs (Nayerossadat et al., 2012). However, due to the fact that high therapeutic doses are required when using non-viral technologies, and the resulting gene expression is generally transient, most gene therapies now rely on viral vectors. Numerous viral vector types have been tested in clinic, including vaccinia, measles, vesicular stomatitis virus (VSV), polio, reovirus, adenovirus, lentivirus, γ-retrovirus, herpes simplex virus (HSV) and adeno-associated virus (AAV) (Lundstrom, 2018).

Objectively Measured Daytime Napping and All-Cause Mortality in Older Adults

Among older adults, longer and more frequent daytime napping, especially in the morning, was associated with higher AllCauseMortality, supporting wearable sleep assessment for risk evaluation.

Question Are objectively measured daytime nap characteristics, including duration, frequency, variability, and timing, associated with all-cause mortality among community-dwelling older adults?

Findings In this prospective cohort study of 1,338 adults aged 56 years or older, longer and more frequent daytime napping, as well as morning napping, were associated with higher all-cause mortality. Variability in nap duration was not associated with mortality.

Meaning The findings suggest longer and more frequent, particularly morning, napping may be a behavioral marker of increased mortality risk in late life, underscoring the potential clinical value of incorporating wearable device–based nap assessments into routine health monitoring.

Protein’s second role in inflammation could reshape treatment for Crohn’s, arthritis and heart disease

A protein long understood to drive inflammation by producing nitric oxide has a second, previously unknown role—it physically binds to another key protein inside cells to directly modulate the immune response. The discovery, published in Nature Metabolism, could open new routes to treating conditions such as cardiovascular disease, arthritis, Crohn’s and other inflammatory diseases.

When the immune system detects infection or injury, it triggers inflammation to fight back. That response is essential, but it must be carefully controlled. If it runs too hard for too long, it causes the tissue damage that underlies many chronic diseases. Understanding the molecular switches that regulate inflammation—and finding new ways to target them—is one of the biggest challenges in modern medicine.

Researchers from the University of Surrey and the University of Oxford have identified one such switch. They have shown that inducible nitric oxide synthase (iNOS)—a protein that produces nitric oxide during inflammation—can also bind directly to a second protein, IRG1, inside mitochondria. That physical interaction blocks IRG1 from producing itaconate, a metabolite that acts as a brake on the inflammatory response.

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