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Kelberman, M.

Publications and source records attributed to Kelberman, M..

3 recordsLinked to original sources

Exploring Synergies in Brain-Machine Interfaces: Compression vs. Performance

Individuals with severe neurological injuries often rely on assistive technologies, but current methods have limitations in accurately decoding multi-degree-of-freedom (DoF) movements. Intracortical brain-machine interfaces (iBMIs) use neural signals to provide a more natural control method, but currently struggle with higher-DoF movements--something the brain handles effortlessly. It has been theorized that the brain simplifies high-DoF movement through muscle synergies, which link multiple muscles to function as a single unit. These synergies have been studied using dimensionality reduction techniques like principal component analysis (PCA), non-negative matrix factorization (NMF), and demixed PCA (dPCA) and successfully used to reduce noise and improve offline decoder stability in non-invasive applications. However, their effectiveness in improving decoding and generalizability for implanted recordings across varied tasks is unclear. Here, we evaluated if brain and muscle synergies can enhance iBMI performance in non-human primates performing a two-DoF finger task. Specifically, we tested if PCA, dPCA, and NMF could compress and denoise brain and muscle data and improve decoder generalization across tasks. Our results showed that while all methods effectively compressed data with minimal loss in decoding accuracy, none improved performance through denoising. Additionally, none of the methods enhanced generalization across tasks. These findings suggest that while dimensionality reduction can aid data compression, alone it may not reveal the "true" control space needed to improve decoder performance or generalizability. Further research is required to determine whether synergies are the optimal control framework or if alternative approaches are required to enhance decoder robustness in iBMI applications. Significance StatementMany researchers believe that brain and muscle synergies represent a fundamental control strategy and could enhance brain-machine interface (BMI) decoding performance. These synergies, extracted through dimensionality reduction techniques, are thought to simplify complex neural data, improving the efficiency and accuracy of BMI systems. In our study, we evaluated brain and muscle synergies in a dexterous finger task. We found that while these synergies effectively compressed high-dimensional data, they did not improve performance through denoising or generalize well across different contexts. Instead, the highest performance was achieved when using all available data, suggesting that synergies, although useful for data compression, may not provide the "true" control space needed to enhance decoder robustness or adaptability in implanted BMI systems.

neuroscience↗

Sparse neural networks enable low-power, implantable neural interfaces

Recent advances in brain-machine interfaces (BMIs) using neural network decoders and increased channel count have improved the restoration of speech and motor function, but at the cost of higher power consumption. For wireless, implantable BMIs to be clinically viable, power consumption must be limited to prevent thermal tissue damage and enable long use without frequent charging. Here, we show how neural network "pruning" creates sparse decoders that require fewer computations and active channels for reduced power consumption. Across multiple movement decoding tasks using brain and muscle signals, recurrent neural network decoders can be compressed by over 100x while maintaining strong performance, enabling decoding on the implant with <1% power increase compared to decoding externally. Pruning also allows for deactivating up to 89% of channels, reducing BMI power by up to 5x. Counterintuitively, our findings suggest that BMIs employing a subset of a larger number of channels may achieve lower power consumption than BMIs with fewer channels, for a given performance level. These results suggest a path toward power-efficient, implantable BMIs suitable for long-term clinical use.

bioengineering↗

Age-dependent dysregulation of locus coeruleus firing in a transgenic rat model of Alzheimers disease

Accumulation of hyperphosphorylated tau in the locus coeruleus (LC) is a ubiquitous feature of prodromal Alzheimers disease (AD), and LC neurons degenerate as AD progresses. Tau-mediated LC dysfunction may contribute to early neuropsychiatric symptoms, while loss of LC integrity is associated with conversion to cognitive impairment. Hyperphosphorylated tau alters firing rates in other brain regions, but its effects on LC neurons have not been described. The purpose of this study was to characterize changes in firing properties of LC neurons when they are the only cells containing hyperphosphorylated tau, as well as later in disease when {beta}-amyloid (A{beta}) and tau pathology is abundant in the forebrain. Single unit LC activity was recorded from anesthetized wild-type (WT) and TgF344-AD rats, which carry the APP/PS1 transgene. Similar to human AD, these rats develop hyperphosphorylated tau in the LC (at 6 months) prior to A{beta} or tau pathology in forebrain regions (at 12-15 months). At baseline, LC neurons from TgF344-AD rats were hypoactive at both ages compared to WT littermates, but showed elevated spontaneous bursting properties, particularly in younger animals. Differences in footshock-evoked LC firing depended on age, with 6-month TgF344-AD rats demonstrating aspects of hyperactivity, and aged transgenic rats showing hypoactivity relative to WT. Tau-induced alterations in LC firing rates may contribute to the pathophysiology of AD, with early hyperactivity associated with prodromal symptoms, followed by hypoactivity contributing to cognitive impairment. These results support further investigation into disease stage-dependent noradrenergic interventions for AD. HighlightsO_LIRecorded locus coeruleus (LC) neurons in a rat model of Alzheimers disease (AD) C_LIO_LITgF344-AD rats develop early endogenous LC tau pathology akin to human AD C_LIO_LI6- and 15-month TgF344-AD rats had reduced tonic LC firing C_LIO_LILC neurons from 6-month TgF344-AD rats were hyperactive in response to footshock C_LIO_LILC neuron dysfunction may contribute to AD symptoms C_LI

neuroscience↗