Northern pike are moving through salt water to invade freshwater habitats in Southcentral Alaska, according to a recent study published in the journal PLOS ONE.

Researchers at the University of Alaska Fairbanks and the Alaska Department of Fish and Game made the discovery by collecting and analyzing tiny ear stones called otoliths from northern pike caught in the region. It's the first known documentation that northern pike are traveling through estuaries, where fresh water from rivers mixes with the ocean, to colonize new territory in North America.

The discovery offers new insights into the ongoing spread of northern pike throughout Southcentral Alaska. A native species in Interior and Western Alaska, northern pike were illegally introduced to the Susitna River basin in the 1950s. Since then, the predatory fish has become established in more than 150 lakes and rivers in the region.

Until now, the spread of northern pike was thought to be limited to freshwater corridors or illegal introductions by people.

"They're a freshwater fish, and it was thought that Cook Inlet represented a marine barrier stopping them from moving from watershed to watershed," said Matthew Wooller, a professor at the UAF College of Fisheries and Ocean Sciences and lead author of the paper.

Wooller, who is also director of the Alaska Stable Isotope Facility at UAF, led the team's efforts to reconstruct the movements of pike by analyzing otoliths collected by ADFG since 2019. The composition of strontium isotopes in the layers of an otolith can be matched with chemical signatures in various waterways, showing where a fish traveled during its life.

"Strontium varies according to geology and location," Wooller said. "If pike are moving between watersheds, you can pick it up by analyzing strontium in the otoliths."

The study found three pike from three separate locations with isotopic signatures matching upper Cook Inlet water, suggesting they had occupied the inlet at some point. Those fish were caught in freshwater habitats that connect to Cook Inlet: Campbell Lake and Westchester Lagoon, both in Anchorage, and Vogel Lake on the Kenai Peninsula. The discovery highlights the steep challenge of limiting the spread of northern pike in the region. It suggests that ocean-connected waterways where northern pike have been eradicated may become reinvaded.

As efficient predators, pike impact native fish species such as salmon when they invade new territory.

The newfound realization that the fish are moving through estuaries "is just one more reason that northern pike are a poster child of what makes a formidable invasive species," said Peter Westley, a UAF associate professor of fisheries who has studied northern pike in their native and introduced ranges for over a decade.

While concerning, the new research also could lead to more targeted action against the invasive fish.

"Confirming northern pike can use this pathway gave us the information we needed to now focus on preventing this spread and protecting valuable habitats," said Parker Bradley, an ADFG invasive species biologist.

Kristine Dunker, who coordinates an ADFG program to manage invasive northern pike in Southcentral Alaska, said "the findings will help direct resources toward monitoring areas without pike that are at the highest risk of invasion.

"This discovery has been a step forward, both scientifically with our understanding of northern pike ecology in North America and also for our invasive northern pike management here at home," Dunker said.

Along with Wooller, Bradley, Dunker and Westley, contributors to the paper included Karen Spaleta at UAF and Robert Massengill, formerly at ADFG.

More information: Matthew J. Wooller et al, Estuarine dispersal of an invasive Holarctic predator (Esox lucius) confirmed in North America, PLOS ONE (2024). DOI: 10.1371/journal.pone.0315320

Journal information: PLoS ONE

Provided by University of Alaska Fairbanks

Brain health: Immune enzyme linked to toxic tau buildup in Alzheimer’s disease

Alzheimer’s disease is one of the world’s biggest health problems. Yet, despite the fact millions of people globally are diagnosed with the disease each year, it remains a challenge to treat. This is largely because the underlying causes are still not fully understood.

However, a new study in mice brings us one step closer to understanding what triggers the disease. The researchers have uncovered a specific enzyme that may be behind one of the key features of Alzheimer’s.

One of the key features of Alzheimer’s disease is an accumulation of a harmful protein called tau. In a healthy brain, tau primarily helps to support and stabilise brain cells (neurons). This maintains the structure of these cells, and assists in transporting key substances throughout the neuron so it can function optimally.

But in people with Alzheimer’s disease, tau appears to behave abnormally in the brain. Instead of performing its normal function, tau builds up inside neurons and forms twisted clumps, called neurofibrillary tangles.

These tangles can disrupt communication between neurons. Communication between neurons is fundamental for our memory, thinking and behaviour, so any disruption can lead to damage in those areas of the brain.

While scientists have known for decades that tau is involved in the disease, they’re still trying to understand exactly why healthy tau misfolds to form these toxic, sticky tangles. This latest study, published in Nature Neuroscience, offers promising new insights into how tau turns toxic in mice. Toxic tau

To mimic Alzheimer’s disease, the team of US-based scientists used mice that had been genetically altered to have a build-up of tau in their brains. They found that a specific enzyme may be responsible for turning healthy tau into the toxic tau that accumulates in the brain.

An enzyme is a protein that usually plays a helpful role in the body – making reactions happen faster and more efficiently. But this study found that the enzyme tyrosine kinase 2 (TYK2), which plays a central role in the immune system, adds a special tag to tau. This tag then appears to make it difficult for the brain to properly clear away unwanted tau. In both mouse models and human cell cultures, the enzyme caused tau to build up and become toxic.

Using genetic tools, the scientists then blocked TYK2 in the mice with Alzheimer’s. This resulted in a reduction in the overall amount of tau in the brain – including the amount of harmful, disease-causing tau with the added tag.

The neurons also showed signs of recovery. This suggests that blocking TYK2 could be a way to reduce the toxic tau buildup, and the damage it causes in diseases like Alzheimer’s. This could also open new avenues for drug development that could tackle toxic tau in ways that haven’t been explored yet.

The finding that lowering or blocking TYK2 could treat Alzheimer’s is encouraging, as TYK2 inhibitor drugs have already been tested in humans for a range of different conditions – such as the autoimmune diseases psoriatic arthritis and inflammatory bowel disease.

However, studies are needed to check if TYK2 inhibitors are able to pass the blood-brain barrier. As tau is inside brain cells, it’s tough to remove. If these drugs can’t reach the brain, they won’t be able to lower tau levels in humans and make a difference in Alzheimer’s disease. Alzheimer’s treatments

There’s a desperate need for new treatment options for Alzheimer’s disease. While two therapies, donanemab and lecanemab, have recently been approved in the UK, they’re too expensive for widespread use on the NHS and come with serious side-effects. Many argue that their drawbacks outweigh their benefits.

These treatments focus on removing amyloid plaques, another protein linked to Alzheimer’s. But targeting tau, the protein at the heart of this new research, could be a game changer in the search for a more effective treatment.

It should, however, be noted that this research is in its early stages and is still very pre-clinical. Despite mice models being extremely valuable for understanding disease mechanisms, their results don’t always translate directly to humans. More research is needed to see if this technique has the same effect on tau levels in the human brain, whether there are any harmful side-effects – and if blocking TYK2 to clear toxic tau actually improves symptoms of Alzheimer’s, such as memory loss.

Targeting TYK2 to reduce toxic tau in the brain shows promise as a potential new approach to treating Alzheimer’s. The next steps will be to explore if the same is true in humans.

The New and Novel Complex Brain-Based Therapy and Jazz

In August 1991, former World Boxing Champion John Famechon sustained severe incapacitating brain injuries. In December of 1993, he began a new and novel complex multi-movement therapy and rehabilitation program, which eventually helped him regain a condition close to his pre-accident state. “The New and Novel Complex Brain Therapy?”

The question to ask and answer was: What was meant by the descriptor “a new and novel therapy?” Which eventually evolved to be described as complex brain-based multi-movement therapy (CBBMMT) and then complex multi-movement therapy (CMMT).

In terms of application, it was my contention that my new and novel therapy had three elements. First, the focus of the therapy was the brain; and it was the application and action of movement that was the only way to access and influence the brain to change, which would then hopefully lead to physical changes taking place.

Second, the aim was to apply as much complexity as possible when visibly feasible. My rationale for this (personal philosophical principle) was that this approach would bring about neurological, neurobiological, and neuromuscular transmission firing, leading to neurological and neuromuscular connections. The hope was that this would lead to neurological and neuromuscular changes, leading to movement returning to limbs that previously were unable to move.

Third, the idea and ongoing hope was to achieve maximum brain and body benefits. That would eventually lead to becoming self-initiated complex brain and body movement. I had no idea if this would happen, but it always made sense to me. My studies in “Play Theory” influenced my thinking about this. Play Theory research declared that play was imperative because when play took place, thinking and movement occurred. This play-based process then changed the brain and continued to develop and advance the fine and gross muscles of the body. This also led to the development and ongoing enhancement of movement and physical skill potential.

The Complex New and Novel Brain-Based Multi-Movement Therapy and Jazz

As I progressed with applying my new and novel complex brain-based multi-movement therapy, its application, and the intuitive movement format I was applying (as time progressed and as I began to see the physical and movement changes taking place, all of this began to remind me of jazz. That idea came to mind because (to my understanding of jazz), that jazz music had, at its essence, the application of instrumental musical intuition. This meant that nothing was planned. The music that came into existence (occurred in the intuitive moment), in accordance with what each musician was hearing and playing.

Jazz is usually improvised (i.e., invented as it is played). However, the musician had to be highly skilled to be able to play the musical instrument in question. This skill level could only be achieved through hard work and unrelenting practice (Alterhaug, 2004; Benson, 2006; Torrance and Schumann, 2019; Zack, 2000).

Jazz is characterised by a strong but flexible rhythmic understructure with solo and ensemble improvisations on basic tunes and chord patterns and, more recently, a highly sophisticated harmonic idiom (Alterhaug, 2004; Benson, 2006; Torrance and Schumann, 2019; Zack, 2000).

Jazz music is (as noted), played by highly skilled and talented musicians in various increasingly complex styles. It is generally marked by intricate, propulsive rhythms, polyphonic ensemble playing, improvisatory, virtuosic solos, melodic freedom, and a harmonic idiom ranging from simple rhythms to complicated atonality (Alterhaug, 2004; Benson, 2006; Torrance and Schumann, 2019; Zack, 2000).

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Plasma Proteomics and social relationships

A new study published in Nature Human Behaviour unveils the intricate biological links between social isolation, loneliness, and a plethora of health outcomes, including cardiovascular disease, diabetes, and mortality. By leveraging data from 42,062 participants in the UK Biobank, the researchers have deciphered plasma proteomic signatures that provide a molecular-level understanding of how social relationships, or the lack thereof, influence human health.

Social connections are fundamental to human survival and well-being, yet modern societies face an increasing prevalence of social isolation and loneliness. These two constructs, while related, represent distinct facets of social disconnection: the former being an objective state of limited social interactions and the latter a subjective feeling of being alone. Both have been empirically linked to increased morbidity and mortality, with effects comparable to traditional risk factors like smoking and obesity. However, the biological mechanisms mediating these associations have remained elusive – until now.

This comprehensive study utilized high-throughput plasma proteomics to explore the proteomic profiles associated with social isolation and loneliness. The findings illuminate shared and distinct molecular pathways, particularly those involving inflammation, antiviral responses, and complement systems, that underlie the health impacts of social disconnection. Furthermore, the study extends beyond correlation, employing Mendelian randomization (MR) to infer causality, thereby identifying five key proteins—GFRA1, ADM, FABP4, TNFRSF10A, and ASGR1—as central mediators in the relationship between loneliness and adverse health outcomes.

Proteins, as the functional products of gene expression, are critical to understanding disease mechanisms and represent prime targets for therapeutic interventions. In this study, 776 proteins were initially associated with social isolation and 519 with loneliness, with 175 and 26 proteins, respectively, maintaining significance after rigorous statistical adjustments. Growth differentiation factor 15 (GDF15), an inflammatory marker, emerged as the most strongly associated protein with social isolation, while proprotein convertase subtilisin/kexin type 9 (PCSK9), a regulator of cholesterol metabolism, was most significantly linked to loneliness. Importantly, over 50% of these proteins were prospectively linked to major diseases and mortality over a 14-year follow-up.

The interplay between these proteins and health was further dissected using protein-protein interaction (PPI) networks and pathway enrichment analyses. Hub proteins such as interleukin 6 (IL6) and intercellular adhesion molecule-1 (ICAM1) were identified, underscoring the pivotal role of immune and inflammatory pathways in the biological impact of social disconnection. Notably, proteins linked to social isolation exhibited enrichment in complement activation and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signaling pathways, while loneliness was associated with metabolic and antiviral processes.

Building on these findings, the study employed MR analysis to infer causal relationships. Loneliness was causally linked to changes in the abundance of five proteins, with ADM and ASGR1 showing strong evidence of colocalization, indicating a shared genetic basis for loneliness and these protein levels. ADM, a protein involved in neuroendocrine stress responses and inflammation, exhibited robust associations with systemic biomarkers such as C-reactive protein (CRP) and brain regions implicated in interoception and emotional processing. These findings highlight ADM’s central role in translating the experience of loneliness into physiological changes that predispose individuals to disease.

The study also explored the mediating role of these proteins in the relationship between loneliness and health outcomes. ADM was identified as a key mediator, explaining up to 16.3% of the excess mortality risk associated with loneliness. The findings suggest that loneliness exerts its health effects not only through behavioral pathways, such as reduced physical activity or unhealthy diets, but also through direct biological mechanisms involving specific proteins and pathways.

To validate these findings, the researchers conducted extensive sensitivity analyses, including stratified analyses by sex, age, and ethnicity, as well as replication in a representative subset of the UK Biobank. The robustness of the results was further supported by cross-validation, colocalization analyses, and mediation modeling. While the study is limited by the observational nature of the data and the inability to measure protein levels in specific tissues, the authors argue that the plasma proteome provides a valuable window into systemic physiological processes.

This research represents a significant leap forward in understanding the biological basis of social relationships and their impact on health. By identifying specific proteins and pathways involved in the effects of social isolation and loneliness, the study opens new avenues for targeted interventions. Potential strategies could include developing drugs that modulate the activity of these proteins, designing biomarkers for early detection of at-risk individuals, or implementing public health policies aimed at reducing social disconnection.

The study underscores the critical importance of social relationships for human health and survival. The proteomic signatures of social isolation and loneliness reveal a complex interplay between biological, psychological, and social factors, offering a comprehensive framework for addressing the health consequences of social disconnection. As societies grapple with the challenges of an increasingly disconnected world, these findings provide a compelling case for prioritizing social relationships as a public health imperative.

Subject of Research: Plasma proteomics and social relationships

Article Title: Plasma proteomic signatures of social isolation and loneliness associated with morbidity and mortality

News Publication Date: 03 January 2025

Article Doi References: 10.1038/s41562-025-00987-5 Image Credits: Not specified

Keywords: Social isolation, Loneliness, Plasma proteomics, Morbidity, Mortality, Inflammation, Mendelian randomization, Public health, Cardiovascular disease, ADM protein

The bacteria behind chlamydia can colonize the gut, and from that hiding place, they may act as a source of repeated infections, new research using miniature intestines suggests.

Chlamydia is the most common sexually transmitted infection (STI) worldwide. The form of the infection that affects humans is caused by a species of bacteria known as Chlamydia trachomatis.

The disease most often affects the genital region, sometimes causing pain and unusual discharge from the vagina or penis. However, over the years, research in mice and various clinical reports in humans have suggested that C. trachomatis may also be able to infect the human digestive tract. This means that, theoretically, the bacteria could hide in the gut and then cause repeated genital infections, which commonly occur in patients despite treatment with antibiotics.

Yet, until now, scientists haven't been able to test this theory in human cells.

Next, they must formulate a research question and design and conduct an experiment in pursuit of an answer.

Then, they must analyse and interpret the results of the experiment, which may raise yet another research question.

Can a process this complex be automated? Last week, Sakana AI Labs announced the creation of an "AI scientist" – an artificial intelligence system they claim can make scientific discoveries in the area of machine learning in a fully automated way.

Key points

• The hippocampus enables abstract reasoning; LLMs mirror this through pattern-based language prediction.
• Future AI could emulate human inference by integrating multimodal learning and reinforcement methods.
• AI's evolution hinges on bridging prediction and reasoning, moving toward deeper, human-like understanding.

Auf dem Prüfstand: Tausende Klimaschutzmaßnahmen wurden bisher in verschiedenen Ländern umgesetzt – aber nur 63 dieser Maßnahmen trugen in größerem Umfang zur Reduktion der globalen Treibhausgas-Emissionen bei, wie eine Auswertung ergab. Der Erfolg dieser Klimapolitik beruht meist auf einer Kombination von Einzelmaßnahmen, die an die Situation des jeweiligen Landes angepasst waren. Was bedeutet dies konkret?

Ob Stürme, Starkregen oder immer neue Temperaturrekorde: Der Klimawandel ist längst konkret spürbar – auch bei uns. Umso dringlicher wird die Frage, wie wir die globale Erwärmung noch aufhalten können. Zwar gibt es schon seit einigen Jahrzehnten Bemühungen, den Ausstoß von Treibhausgasen zu verringern und von fossilen Brennstoffen auf erneuerbare Energien umzusteigen. In einigen Ländern haben solche Klimaschutzmaßnahmen auch schon erste positive Wirkungen gezeigt. Sie reichen aber nicht aus, um den globalen Klimawandel zu bremsen oder gar zu stoppen.

Das wirft die Frage auf, welche der bisher in verschiedenen Ländern umgesetzten Klimaschutz-Maßnahmen überhaupt wirksam sind und die CO2-Emissionen effektiv senken.

A new study published in Nature Microbiology has pioneered the use of a single-celled parasite, Toxoplasma gondii, to inject therapeutic proteins into brain cells. The brain is very picky about what it lets in, including many drugs, which limits treatment options for neurological conditions.

As a professor of microbiology, I’ve dedicated my career to finding ways to kill dangerous parasites such as Toxoplasma. I’m fascinated by the prospect that we may be able to use their weaponry to instead treat other maladies.

By using brain organoids derived from autistic children’s stem cells, researchers uncovered distinct neural growth patterns, potentially guiding personalized treatments and diagnoses.

Details of the model, which is called RTDetective, are provided in a new paper published in Nature Genetics titled, “Genome-scale quantification and prediction of pathogenic stop codon readthrough by small molecules.” Its developers believe that the tool could be helpful in the design, development, and efficacy of clinical trials of drugs referred to as nonsense suppression therapies.

Understanding these drugs requires some background on truncated protein translation due to premature termination codons. This phenomenon has been linked to approximately 10–20% of inherited diseases including some types of cystic fibrosis and Duchenne muscular dystrophy. It is also a major mechanism by which tumor suppressor genes are inactivated in cancer.