Naturalized alien plants, also known as neophytes, can have major impacts on the affected regions’ ecosystems. This is particularly evident in the case of invasive plants, which are spreading rapidly in new regions and outcompete the native flora. But what makes these plants so successful? Is it because they are exploiting an “ecological gap” in the foreign ecosystem, allowing them to thrive so easily? Or are they simply “naturally” good at expanding their range? In other words: Do plant species that are on the rise in their native habitats also become globally widespread as naturalized aliens?

Led by the University of Konstanz, an international research team found clear evidence supporting this theory. Their study compared the spread of 3,920 native plant species in ten European countries with how widely these species are naturalized globally. Europe is one of the world’s “main exporters” of naturalized plants. “Our results show that many of the European plant species that successfully naturalize in foreign ecosystems are species that have expanded rapidly in their European home regions as well,” explains Konstanz biologist Mark van Kleunen, who led the study. “Plants that are declining in their natural range, on the other hand, rarely succeed in settling in foreign areas.”

The results of the study indicate that it could be the same characteristics that make plants successful both in their homelands and in foreign regions. The researchers identified common characteristics of these species: “In general, they are tall, ecologically versatile generalists that are highly competitive and prefer nutrient-rich habitats,” summarizes Rashmi Paudel, first author of the study.

“If the plant species that are widespread and on the rise within their native habitats are essentially the same as those that spread successfully – and sometimes become invasive – in other regions of the world, then it stands to reason that both processes are at least based on similar biological mechanisms,” concludes Paudel. “This could reflect that the selective pressures that have made certain species common in their native regions also have preadapted them for success as invaders. This could also reflect that such common species were more likely to be picked up, transported and introduced elsewhere.” Observing the dynamics of the spread of native plants at home can thus provide valuable indications for assessing the likelihood of their establishment in new territories.

“This study shows that air pollution doesn’t just increase the risk of dementia — it actually makes Alzheimer’s disease worse,” said Edward Lee, MD, PhD, co-director of Penn’s Institute on Aging. “As researchers continue to search for new treatments, it’s important to uncover all of the factors that contribute to the disease, including the influence of the environment in which they live.”

Health risks from tiny air particles

Air pollution is made up of fine particulate matter, or the tiny, inhalable particles, ranging from 10 micrometers to less than 2.5 micrometers wide, about half the width of a single strand of spider web. It can come from wildfire smoke, car exhaust, construction site debris, or combustion from factories. Particulate matter 2.5 micrometers and smaller (PM_2.5) is so small that when inhaled, the particles can be absorbed into the blood stream and cause health concerns. Previous research has linked air pollution containing PM_2.5 with dementia, loss of cognitive function, and accelerated cognitive decline.

The researchers examined brain samples from over 600 autopsies from the Penn Medicine Brain Bank. Using data from satellites and local air quality monitors, the researchers modeled the amount of PM_2.5 in the air based on where each person lived. They found that for every increase of 1 microgram per cubic meter of PM_2.5, the risk for worse Alzheimer’s disease amyloid and tau buildup increased by 19 percent.

Further, when they examined the clinical records of these individuals, researchers found that those who lived in areas with high concentrations of PM_2.5 with advanced pathology also had greater cognitive impairment and more rapid onset of symptoms, including memory loss, difficulty with speech, and diminished judgement, compared to people who lived in areas with lower concentrations of air pollution.

While this study focused on exposures to PM_2.5 based on geographic location, researchers acknowledgethat they could not account for individual-specific exposures to air pollution, such as exposure to second-hand smoke in the home, or working with potentially dangerous chemicals.

“In the United States, air pollution is at the lowest levels in decades, but even just a year living in an area with high levels of pollution can have a big impact on a person’s risk for developing Alzheimer’s disease,” said Lee. “It underscores the value of environmental justice efforts that focus on reducing air pollution to improve public health.”

This research is funded by the National Institutes of Health and the National Institute of Environmental Health Sciences (P30AG072979, P01AG066597, U19AG062418, P01AG084497, and P30ES013508).

But why lack of sleep — in particular the early, deep phase called non-REM sleep — lowers levels of growth hormone has been a mystery.

In a study published in the current issue of the journal Cell, researchers from University of California, Berkeley, dissect the brain circuits that control growth hormone release during sleep and report a novel feedback mechanism in the brain that keeps growth hormone levels finely balanced.

The findings provide a map for understanding how sleep and hormone regulation interact. The new feedback mechanism could open avenues for treating people with sleep disorders tied to metabolic conditions like diabetes, as well as degenerative diseases like Parkinson’s and Alzheimer’s.

“People know that growth hormone release is tightly related to sleep, but only through drawing blood and checking growth hormone levels during sleep,” said study first author Xinlu Ding, a postdoctoral fellow in UC Berkeley’s Department of Neuroscience and the Helen Wills Neuroscience Institute. “We’re actually directly recording neural activity in mice to see what’s going on. We are providing a basic circuit to work on in the future to develop different treatments.”

Because growth hormone regulates glucose and fat metabolism, insufficient sleep can also worsen risks for obesity, diabetes and cardiovascular disease.

The sleep-wake cycle

The neurons that orchestrate growth hormone release during the sleep-wake cycle — growth hormone releasing hormone (GHRH) neurons and two types of somatostatin neurons — are buried deep in the hypothalamus, an ancient brain hub conserved in all mammals. Once released, growth hormone increases the activity of neurons in the locus coeruleus, an area in the brainstem involved in arousal, attention, cognition and novelty seeking. Dysregulation of locus coeruleus neurons is implicated in numerous psychiatric and neurological disorders.

“Understanding the neural circuit for growth hormone release could eventually point toward new hormonal therapies to improve sleep quality or restore normal growth hormone balance,” said Daniel Silverman, a UC Berkeley postdoctoral fellow and study co-author. “There are some experimental gene therapies where you target a specific cell type. This circuit could be a novel handle to try to dial back the excitability of the locus coeruleus, which hasn’t been talked about before.”

The researchers, working in the lab of Yang Dan, a professor of neuroscience and of molecular and cell biology, explored the neuroendocrine circuit by inserting electrodes in the brains of mice and measuring changes in activity after stimulating neurons in the hypothalamus with light. Mice sleep for short periods — several minutes at a time — throughout the day and night, providing many opportunities to study growth hormone changes during sleep-wake cycles.

Using state-of-the-art circuit tracing, the team found that the two small-peptide hormones that control the release of growth hormone in the brain — GHRH, which promotes release, and somatostatin, which inhibits release — operate differently during REM and non-REM sleep. Somatostatin and GHRH surge during REM sleep to boost growth hormone, but somatostatin decreases and GHRH increases only moderately during non-REM sleep to boost growth hormone.

Released growth hormone regulates locus coeruleus activity, as a feedback mechanism to help create a homeostatic yin-yang effect. During sleep, growth hormone slowly accumulates to stimulate the locus coeruleus and promote wakefulness, the new study found. But when the locus coeruleus becomes overexcited, it paradoxically promotes sleepiness, as Silverman showed in a study published earlier this year.

“This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness,” Silverman said. “Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair and metabolic health.”

Because growth hormone acts in part through the locus coeruleus, which governs overall brain arousal during wakefulness, a proper balance could have a broader impact on attention and thinking.

“Growth hormone not only helps you build your muscle and bones and reduce your fat tissue, but may also have cognitive benefits, promoting your overall arousal level when you wake up,” Ding said.

The work was funded by the Howard Hughes Medical Institute (HHMI), which until this year supported Dan as an HHMI investigator, and the Pivotal Life Sciences Chancellor’s Chair fund. Dan is the Pivotal Life Sciences Chancellor’s Chair in Neuroscience. Other co-authors of the paper are Peng Zhong, Bing Li, Chenyan Ma, Lihui Lu, Grace Jiang, Zhe Zhang, Xiaolin Huang, Xun Tu and Zhiyu Melissa Tian of UC Berkeley; and Fuu-Jiun Hwang and Jun Ding of Stanford University.

Approximately one in three Americans reports experiencing overwhelming drowsiness during the day — a condition known as excessive daytime sleepiness (EDS). EDS is linked to an increased risk of serious conditions such as cardiovascular disease, obesity, and diabetes. A new study led by investigators from Mass General Brigham and Beth Israel Deaconess Medical Center identifies several molecules in the blood, known as metabolites, that are linked to EDS. Findings suggest that risk of the condition may be influenced by both internal body processes, such as hormone levels, and external factors such as diet. Results are published in Lancet eBioMedicine.

“Our study suggests diet and genetics may play an important role in EDS,” said lead author Tariq Faquih, PhD, a postdoctoral fellow in the Division of Sleep and Circadian Disorders at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “As we learn what’s happening biologically, we are beginning to understand how and why EDS occurs, the early signs that someone might have it, and what we can do to help patients.”

Researchers collected data on 877 metabolites, naturally occurring molecules in the body influenced by diet and hormones. The team used blood samples from 6,000 participants in the Hispanic Community Health Study/Study of Latinos. The team also used data from a questionnaire that assesses how often a person dozes off during the day in various scenarios. The team replicated the findings in The Multi-Ethnic Study of Atherosclerosis (MESA) study and studies in the UK and Finland.

They identified seven metabolites associated with EDS. An additional three metabolites were identified that varied by sex. The team found that omega-3 and omega-6 fatty acids, which are commonly found in foods that make up Mediterranean-like diets, were associated with lower risk of EDS. Other metabolites, such as tyramine, which is found in fermented and overripe foods, were associated with increased daytime sleepiness, particularly in men. Sex steroid metabolites, such as progesterone, were associated with sleep-related processes such as melatonin production.

Researchers note that the results suggest potential treatment targets for EDS and that dietary changes or medications may lead to better treatment. They also note some limitations to the study, including difficulty in interpreting exact values of metabolites and using a sleep questionnaire instead of bringing participants into a sleep lab for tests.

Future directions could include conducting a clinical trial to see if dietary changes or supplements can help reduce daytime sleepiness. Additionally, the authors identified some unknown metabolites that they plan to explore further.

“Conducting a clinical trial would be a big next step and could help us understand if omega-3s and omega-6s obtained from diet could help lower risk of EDS,” said Faquih.

Authorship: In addition to Faquih, MGB authors include Kaitlin S. Potts, Pavithra Nagarajan, Hanna M. Ollila, Tianyi Huang, Clary B. Clish, Susan Redline, Tamar Sofer, and Heming Wang.

Disclosures: Redline discloses consulting relationships with Eli Lilly Inc., Jazz Pharma, and Apnimed Inc. Additionally, Redline serves as an unpaid board member for the Alliance for Sleep Apnoea Partners and has received loaned equipment for a multi-site study: oxygen concentrators from Philips Respironics and polysomnography equipment from Nox Medical.

Funding: This study was funded by the National Institutes of Health (R01HL153814, R01HL161012 and 7R01HL161012) and the JLH Foundation.

Study lead author Dr Maria Randazzo, an academic from CDU’s School of Law, found the technology was reshaping Western legal and ethical landscapes at unprecedented speed but was undermining democratic values and deepening systemic biases.

Dr Randazzo said current regulation failed to prioritize fundamental human rights and freedoms such as privacy, anti-discrimination, user autonomy, and intellectual property rights – mainly thanks to the untraceable nature of many algorithmic models.

Calling this lack of transparency a “black box problem,” Dr Randazzo said decisions made by deep-learning or machine-learning processes were impossible for humans to trace, making it difficult for users to determine if and why an AI model has violated their rights and dignity and seek justice where necessary.

“This is a very significant issue that is only going to get worse without adequate regulation,” Dr Randazzo said.

“AI is not intelligent in any human sense at all. It is a triumph in engineering, not in cognitive behavior.

“It has no clue what it’s doing or why – there’s no thought process as a human would understand it, just pattern recognition stripped of embodiment, memory, empathy, or wisdom.”

Currently, the world’s three dominant digital powers – the United States, China, and the European Union – are taking markedly different approaches to AI, leaning on market-centric, state-centric, and human-centric models respectively.

Dr Randazzo said the EU’s human-centric approach is the preferred path to protect human dignity but without a global commitment to this goal, even that approach falls short.

“Globally, if we don’t anchor AI development to what makes us human – our capacity to choose, to feel, to reason with care, to empathy and compassion – we risk creating systems that devalue and flatten humanity into data points, rather than improve the human condition,” she said.

“Humankind must not be treated as a means to an end.”

“Human dignity in the age of Artificial Intelligence: an overview of legal issues and regulatory regimes” was published in the Australian Journal of Human Rights.

The paper is the first in a trilogy Dr Randazzo will produce on the topic.