NR Times explores the latest research developments in the world of neurorehabilitation
Brain stimulation improves vision recovery after stroke
Hemianopia is a condition that causes loss of half of the visual field (the “vertical midline”), which can happen following stroke and can severely affect daily activities such as reading, driving, or just walking through a crowded space.
There are currently no treatments that can restore lost visual function in hemianopia satisfactorily. Most available options focus on teaching patients how to adapt to loss of vision rather than recovering it. To achieve some degree of recovery, months of intensive neurorehabilitative training are required for only moderate restoration at best.
Researchers led by Friedhelm Hummel at EPFL’s Neuro-X Institute have now tested a new treatment that combines visual training with a multifocal, non-invasive brain stimulation approach to re-orchestrate brain communication and improve recovery in hemianopia.
The research shows that this new approach can significantly enhance recovery of visual functions in stroke patients, even those with long-standing visual impairments.
The trial enrolled 16 stroke patients with hemianopia. The participants trained on a motion-detection task designed to stimulate the edge of their blind field.
At the same time, they received a type of brain stimulation called cross-frequency transcranial alternating current stimulation (cf-tACS), which uses low-intensity electrical currents to modulate brain oscillations, re-orchestrate them and enhance cognitive functions.
In this study, cf-tACS was used to synchronize brain oscillations between the primary visual cortex and the medio-temporal area.
The researchers applied electrical signals at different frequencies to these two areas in a way that mimicked the brain’s natural communication pattern.
The team used a forward-pattern cf-tACS, which delivers low-frequency alpha waves to the primary visual cortex and high-frequency gamma waves to the motion-sensitive area.
This approach mirrors the brain’s typical “bottom-up” information flow during visual processing, helping to re-establish disrupted communication after stroke.
The patients who received the forward-pattern cf-tACS showed significantly greater improvements in motion perception than those who received the reverse-pattern control.
Patients experienced measurable expansions in their visual fields, particularly in the areas that were targeted during training.
Some patients even reported real-world improvements, such as one being “able to see the right arm of his wife when seated on the passenger seat, when she is driving”, which was impossible before the cf-tACS treatment.
Brain imaging and EEG data confirmed that the treatment restored communication between the primary visual cortex and the medio-temporal area.
EEG revealed improved synchronization between these regions, and brain scans confirmed increased activity in the medio-temporal area after stimulation.
The strongest improvements were seen in patients whose visual cortex-to-medio-temporal area pathways were still partly intact, suggesting that even partial preservation of these circuits can support recovery.
This study shows that targeting specific brain circuits with synchronized, physiology-inspired stimulation can amplify the effects of visual training.
If confirmed in larger trials, the approach could offer a faster, more accessible therapy for stroke survivors who suffer hemianopia.
Next-generation microbiome medicine may revolutionise Parkinson’s treatment
Researchers have engineered a groundbreaking living medicine which is a beneficial probiotic designed to deliver Levodopa steadily from the gut to the brain of Parkinson’s patients.
The team engineered and tested the probiotic bacterium Escherichia coli Nissle 1917 as a drug-delivery system that continuously produces and delivers the gold-standard Parkinson’s drug, which is converted to dopamine in the brain.
E. coli Nissle strain was chosen for its century-long record of safely treating gastrointestinal disorders in humans.
Parkinson’s is caused by the loss of dopamine-producing nerve cells in the brain.
Dopamine is a neurotransmitter that governs movement and other functions.
Levodopa (L-DOPA), as a pill, has been used for decades to treat the motor symptoms of Parkinson’s, such as slow movement, tremor, rigidity, and balance problems.
Ironically, prolonged use of the drug can cause an unpredictable return of motor symptoms requiring multiple daily doses.
Over time, this can lead to dyskinesia, characterised by involuntary movements of the neck, trunk, limbs, and face.
Dyskinesia, often mistaken for a symptom of Parkinson’s, is caused by L-DOPA entering the blood in waves, causing ups and downs in brain dopamine levels between doses.
Developing “living drugs” has implications for treating neurological and related gastrointestinal diseases, such as Crohn’s.
The efforts unite microbiologists and neuropharmacologists to research the causes and treatments for such illnesses.
The team say that the preclinical findings for this L-DOPA engineered live-biotherapeutic suggest they are ready for testing in human clinical trials.
What can polymers teach us about curing Alzheimer’s disease?
Researchers from Tokyo Metropolitan University have applied ideas from polymer physics to illuminate the mechanism behind a key pathology in Alzheimer’s disease, the formation of fibrils of tau proteins.
The team showed that fibril formation is preceded by the birth of large protein clusters, mirroring the crystallization of polymers.
Crucially, dissolving these clusters helped to prevent fibrils forming in solution. Their work signals a paradigm shift for the development of treatments for neurodegenerative diseases.
Alzheimer’s disease (AD) continues to present an immense challenge to scientists, both in understanding its progression and developing effective treatments.
With populations aging worldwide, the stakes couldn’t be higher.
Most approaches have been through the lens of pharmacology and medical science; given the sheer complexity of the disease, adjacent disciplines have become increasingly important in presenting fresh research directions and insights.
Now, a team led by Professor Rei Kurita from Tokyo Metropolitan University have used approaches based on polymer physics to understand one of the key pathologies of AD, the formation of fibrils of the tau protein.
They were inspired by the hierarchical process by which polymers, long chain-like molecules, form well-ordered crystals.
Instead of individual strands joining onto crystals in a step-by-step fashion, many polymers create intermediate, “precursor” structures before the rearrangements required to form crystals.
Applying these ideas to the human tau protein in solution, they were able to confirm that the birth of fibrils (or fibrillization) is preceded by the formation of a similar precursor structure, a loose clustering of tau protein with dimensions of tens of nanometers.
They were able to confirm these structures using independent techniques, such as small angle X-ray scattering and fluorescence-based methods.
Crucially, they were able to show that these precursors were not solid, but loose, transient structures which could be dissolved by changing the amount of sodium chloride in the presence of heparin, a naturally occurring anticoagulant in the human body.
Solutions which had these cluster structures dissolved or suppressed showed nearly no formation of fibrils.
The team proposed a mechanism by which the interaction between heparin and tau protein in the solution was reduced, making it harder to form clusters; the higher concentration of charged ions led to charged molecules like tau and heparin being more effectively hidden from each other through a process known as electrostatic “screening.”
The team’s findings suggest an entirely new paradigm for developing treatments, where one might target the reversible formation of precursors instead of trying to disassemble the final fibres.
This is a crucial step forward for not only understanding and treating AD, but a wider range of neurodegenerative diseases, including Parkinson’s disease.
