Round up: Scientists reverse Alzheimer’s in mice using nanoparticles, and more
NR Times explores the latest research developments in the world of neurology and neurorehabilitation.
Scientists reverse Alzheimer’s in mice using nanoparticles
Researchers have demonstrated a nanotechnology strategy that reverses Alzheimer’s disease in mice.
Unlike traditional nanomedicine, which relies on nanoparticles as carriers for therapeutic molecules, this approach employs nanoparticles that are bioactive in their own right: “supramolecular drugs.”
Instead of targeting neurons directly, the therapy restores the proper function of the blood-brain barrier (BBB), the vascular gatekeeper that regulates the brain’s environment. By repairing this critical interface, the researchers achieved a reversal of Alzheimer’s pathology in animal models.
The brain is the most expensive organ of the body, consuming 20 per cent of the energy in adults and up to 60 per cent in children. This energy arrives through a vast blood supply, assured by a unique and dense vascular system where each neuron is nourished by one capillary.
Our brain contains approximately one billion capillaries, highlighting the vital role of brain vasculature in maintaining health and combating disease. These findings highlight the crucial role of vascular health, especially in diseases like dementia and Alzheimer’s, where a compromised vascular system is closely linked.
The BBB is a cellular and physiological barrier that separates the brain from the blood flow to protect it from external dangers such as pathogens or toxins.
The team demonstrated that targeting a specific mechanism enables undesirable “waste proteins” produced in the brain to pass through this barrier and be eliminated in the blood flow.
In Alzheimer’s disease, the main “waste” protein is amyloid-β (Aβ), whose accumulation impairs the normal functioning of the neurons.
Researchers used mouse models that are genetically programmed to produce larger amounts of Aβ protein and develop a significant cognitive decline mimicking Alzheimer’s pathology.
They administered only three doses of the supramolecular drugs and afterwards regularly monitored the evolution of the disease.
“Only one hour after the injection we observed a reduction of 50 to 60 per cent in Aβ amount inside the brain” said Junyang Chen, first co-author of the study, researcher at the West China Hospital of Sichuan University and PhD student at the University College London (UCL).
The most striking data were the therapeutic effects. Researchers conducted various experiments to analyse the behaviour of the animals and measure their memory decline over several months, covering all stages of the disease.
In one of the experiments, they treated a 12-month-old mouse (equivalent to a 60-year-old human) with the nanoparticles and analysed its behaviour after six months. The result was impressive: the animal, aged 18 months (comparable to a 90-year-old human), had recovered the behaviour of a healthy mouse.
Giuseppe Battaglia, ICREA research professor at IBEC and principal investigator of the Molecular Bionics Group and leader of the study, said: “The long-term effect comes from restoring the brain’s vasculature. We think it works like a cascade: when toxic species such as amyloid-beta (Aβ) accumulate, disease progresses.
“But once the vasculature is able to function again, it starts clearing Aβ and other harmful molecules, allowing the whole system to recover its balance. What’s remarkable is that our nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels.”
TBI in older adults linked to increased risk of dementia
Traumatic brain injuries (TBI) in older adults are associated with new cases of dementia, use of home care services, and admission to long-term care, new research shows.
To understand the impact of late-life TBI and the association with new cases of dementia and related care needs, researchers analysed data on more than 260 000 adults aged 65 years or older with and without TBI between April 2004 and March 2020.
The study followed participants until a diagnosis of dementia, to March 2021, or death.
New TBI was associated with a 69 per cent increased risk of subsequent dementia in the first 5 years, a 56 per cent increased risk beyond five years, and more days of publicly funded home care, at 87 days compared with 84 days in people without TBI).
Age and female sex were associated with higher risk of dementia, with about one in three people aged 85 years and older predicted to develop dementia after TBI.
Income was also linked to dementia risk, with people from low-income neighbourhoods at higher risk of dementia than those in high-income neighbourhoods. People living in smaller communities, low-income regions, and areas with less ethnic diversity were more likely to be admitted to a long-term care facility.
Creative experiences delay brain ageing
A new, international study has revealed that engaging in creative experiences such as music, dance, visual arts, and even specific video games can slow brain ageing and promote healthier brain function.
Although creativity has long been celebrated for its cultural and personal value, this study is the first large-scale scientific evidence directly linking creative engagement to direct measurable protection of brain health.
Researchers across 13 countries, including researchers from Trinity College Dublin, examined brain data from more than 1,400 participants, including creative experts like tango dancers, musicians, visual artists, learners and non-experts.
They found that sustained engagement in creative activities was consistently associated with “younger” brains, while even short-term training produced measurable (though smaller) benefits.
Dr. Agustin Ibanez, senior and corresponding author of the study, and professor in brain health at the Global Brain Health Institute and School of Medicine, Trinity College Dublin, said “Creativity emerges as a powerful determinant of brain health, comparable to exercise or diet.
“Our results open new avenues for creativity-based interventions to protect the brain against aging and disease.
“Our study also showed that brain clocks can be used to monitor interventions aimed to improve brain health.”
So far, “brain clocks” have primarily been used to assess the negative influences on brain health, including genetic risks, environmental exposures (the exposome), and social inequalities.
This is one of the few studies that demonstrates, for the first time, that brain clocks can also capture positive influences – in this case, the protective impact of creativity.
Results showed that creativity was consistently linked to younger brain profiles. The protective effects were most evident in regions vulnerable to neurodegeneration such as the hippocampus, prefrontal cortex and parietal areas.
Computational modeling revealed that creative engagement supports more efficient brain networks and stronger connectivity, mechanisms believed to underlie its protective role.
The findings highlight creativity as a public health resource, with implications for clinical interventions and health policy. From tango to video gaming, creative practices share common benefits for brain health and healthy ageing.
Outdoor air exposure to chemical may raise risk of Parkinson’s disease
Long-term exposure to the industrial solvent trichloroethylene (TCE) outdoors may be linked to an increased risk of Parkinson’s disease, according to a large nationwide US study.
Trichloroethylene is a chemical used in metal degreasing, dry cleaning and other industrial applications. Although TCE has been banned for certain uses, it remains in use today as an industrial solvent and is a persistent environmental pollutant in air, water and soil across the United States.
The study does not prove that TCE exposure causes Parkinson’s disease, it only shows an association.
Researchers used Medicare data to identify people over age 67 newly diagnosed with Parkinson’s between 2016 and 2018. Each person was compared with five people who did not have the disease. The study included 221,789 people with Parkinson’s and over 1.1 million people without the disease.
The study mapped exposure to outdoor TCE concentrations using US Environmental Protection Agency data and participants’ residential neighborhood based on their ZIP +4 location. Air levels of TCE were estimated by US Census tract, a small area within a county. Each participant’s exposure was based on their neighborhood two years prior to diagnosis.
Researchers divided participants into 10 groups based on their estimated TCE exposure. Those in the lowest exposure group experienced levels between 0.005 and 0.01 micrograms per cubic meter (μg/m³), while those in the highest group had exposures ranging from 0.14 to 8.66 μg/m³.
After adjusting for other factors that could affect the risk of Parkinson’s, including age, smoking history and exposure to fine particulate air pollution, researchers found people exposed to the highest outdoor TCE levels had a 10 per cent increased risk of Parkinson’s disease compared to people exposed to the lowest levels.
The researchers also identified several geographic “hot spots” where outdoor TCE levels were highest, particularly in the Rust Belt region of the US and smaller pockets across the country.
They then analysed Parkinson’s risk in the 10 miles surrounding the three top TCE-emitting facilities in the US from 2002. For two of the areas, risk was higher closer to the facilities, and at one of those sites, there was a clear increasing incremental risk the closer people lived to the facility.
A limitation of the study is that it focused only on Medicare-aged individuals, so findings may not apply to younger people or those with early-onset Parkinson’s disease. In addition, TCE exposure estimates were based on outdoor air levels in 2002 and may not reflect individual lifetime or indoor exposures.
