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Barron, J. C.

Publications and source records attributed to Barron, J. C..

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Proteomic profiling of baseline CSF and serum from HDClarity identifies signatures for Huntington disease staging and stratification

Background: Sensitive biomarkers that objectively stage Huntington disease (HD) are needed to improve participant stratification and facilitate the enrichment of clinical trials with biologically and clinically homogeneous populations. The HDClarity study, an international longitudinal biofluid collection initiative for HD, provides a unique resource for large-scale proteomic profiling of matched CSF and serum samples from healthy controls and individuals across premanifest and manifest stages of HD. Here, we leveraged baseline proteomic data from HDClarity to characterize protein signatures associated with disease stage and clinical severity, compare measurements across analytical platforms and biofluid compartments, and identify candidate multi-protein panels for disease staging. Methods: Baseline proteomic data generated using Olink Explore (~3,000 proteins) and SomaScan (~7,000 proteins) were analyzed in matched CSF and serum samples from 315 HD gene-expansion carriers and 92 non-HD controls. A total of 2,119 proteins overlapped between Olink and SomaScan, enabling assessment of cross-platform concordance, while CSF-serum relationships were evaluated using all available protein measurements within each assay. Covariate-adjusted linear regression models were used to assess disease stage-associated differences in protein abundance, while partial correlation analyses evaluated relationships between protein abundance, clinical severity in HD gene-expansion carriers, and estimated years to disease onset in premanifest participants. A nested machine-learning pipeline incorporating univariate feature ranking, penalized regression-based feature selection, and repeated cross-validation was used to derive compact multi-protein classifiers for HD staging. Results: Cross-platform and CSF-serum correlations were highly protein-dependent, with some analytes showing strong concordance and others exhibiting weak or inverse relationships. These findings highlight substantial heterogeneity in biomarker behaviour across analytical platforms and biofluids. Adjusted models identified both known HD-associated markers (NEFL, GFAP, CHI3L1) and less well-characterized proteins in CSF (TNFRSF8, TPM3, NPPB) and serum (OMG, NPTXR, NCAN) whose baseline abundance differed across clinical and/or HD-Integrated Staging System (HD-ISS) stages. Partial correlation analyses revealed additional candidate biomarkers associated with clinical severity and years to predicted disease onset. Machine-learning models identified compact CSF and serum protein panels that achieved high classification accuracy (AUC > 0.9) across all clinical contrasts, with models distinguishing the transitions from HD-ISS stage 0 to 1 and from premanifest to early manifest disease demonstrating robust generalization to unseen data. Conclusions: This study provides the first large-scale comparison of matched CSF and serum proteomic profiles from the HDClarity cohort, identifying robust baseline proteomic signatures across the HD continuum. Our findings demonstrate the importance of considering both analytical platform and biofluid when interpreting protein biomarkers and identify compact protein panels with potential utility for objective disease staging, patient stratification, and clinical trial enrichment in HD.

neuroscience↗

Striatal neuron excitability is regulated by huntingtin in the adult brain

Huntingtons disease (HD) is a hereditary neurodegenerative disease that typically presents during midlife and is characterized by a combination of motor, cognitive and psychiatric symptoms. HD is fatal and arises from a mutation in the huntingtin (HTT) gene, which results in decreased neuronal health followed by brain atrophy, with spiny projection neurons (SPNs) of the striatum being especially vulnerable to degeneration. HTT loss-of-function, caused by haploinsufficiency of the wild type HTT gene (wtHTT), is an important feature of HD pathophysiology that has previously been understudied compared to mutant HTT gain-of-function mechanisms. wtHTT is essential for nervous system development and functions as a scaffolding protein to support many vital cellular functions including axonal transport, autophagy and synaptic plasticity. Here, we examined the consequences of wtHTT deletion in the adult striatum by conditionally inactivating wtHTT in 2-4 month old male and female Httfl/fl mice. wtHTT loss of function in mature SPNs decreased intrinsic neuronal excitability and produced a neuroinflammatory response in these mice, while tissue organization, spine morphology and motor behaviour remained unaffected. Results presented here provide additional evidence that wtHTT is vital for maintaining neuronal health in the adult brain and highlight some potential adverse consequences of non-selective HTT-lowering for the treatment of HD.

neuroscience↗

Emergent glutamate & dopamine dysfunction in VPS35(D620N) knock-in mice and rapid reversal by LRRK2 inhibition

The D620N variant in Vacuolar Protein Sorting 35 (VPS35) causes autosomal-dominant, late- onset Parkinsons disease. VPS35 is a core subunit of the retromer complex that canonically recycles transmembrane cargo from sorting endosomes. Although retromer cargoes include many synaptic proteins, VPS35s neuronal functions are poorly understood. To investigate the consequences of the Parkinsons mutation, striatal neurotransmission was assessed in 1-, 3- & 6-month-old VPS35 D620N knock-in (VKI) mice. Spontaneous and optogenetically- evoked corticostriatal glutamate transmission was increased in VKI striatal spiny projection neurons by 6 months, when total striatal glutamate release, quantified by iGluSnFR imaging, showed similarities to wild-type. dLight imaging revealed robust increases in VKI striatal dopamine release by 6 months, which were reversed with acute ex vivo leucine-rich repeat kinase 2 (LRRK2) inhibition. We conclude that increased glutamate and dopamine transmission in VKI mice progressively emerges in young-adulthood, and that dopamine dysfunction is likely the result of sustained, rapidly-reversible, LRRK2 hyperactivity.

neuroscience↗

Huntingtin is essential for synaptic plasticity in the adult hippocampus

Huntingtin (HTT), an exceptionally large protein with hundreds of interacting partners within the central nervous system, has been extensively studied due to its role in Huntingtons disease (HD) pathology. HD is a monogenic disorder caused by a polyglutamine repeat expansion in the HTT gene, which results in the production of a pathogenic mutant huntingtin (mHTT) protein, and toxic effects of this mutant protein in the context of HD have been well-established. Less-established, however, is the role of wild type HTT (wtHTT) in the adult brain, particularly in areas outside the corticostriatal pathway. wtHTT has previously been suggested to play a vital role in cellular functions that promote synapse homeostasis, such as fast axonal transport of synaptic cargo, vesicle replenishment and receptor localization and stability. Synaptic dysfunction precedes and predicts cell death in many neurodegenerative diseases including HD (termed synaptopathies) and whether proper synaptic transmission can be maintained without wtHTT in extrastriatal brain areas such as the hippocampus remains unknown. Consequences of wtHTT reduction in the adult brain are of particular importance as clinical trials for many non-selective HTT-lowering therapies for HD are underway, which are unable to distinguish between mHTT and wtHTT, and therefore reduce levels of both proteins. We investigated the consequences of wtHTT loss of function in the CA3-CA1 pathway of the adult hippocampus using a conditional knockout mouse model and found that 1-2 month deletion of wtHTT in excitatory hippocampal neurons inhibits post-tetanic potentiation and completely abolishes NMDA receptor-dependent long-term potentiation in these animals. These data reveal a novel role of wtHTT as an essential regulator of short- and long-term plasticity in the adult hippocampus.

neuroscience↗

Asymmetric dysregulation of glutamate dynamics across the synaptic cleft in a mouse model of Alzheimer disease

Most research on glutamate spillover focuses on the deleterious consequences of postsynaptic glutamate receptor overactivation. However, two decades ago, it was noted that the glial coverage of hippocampal synapses is asymmetric: astrocytic coverage of postsynaptic sites exceeds coverage of presynaptic sites by a factor of four. The fundamental relevance of this glial asymmetry remains poorly understood. Here, we used the glutamate biosensor iGluSnFR, and restricted its expression to either CA3 or CA1 neurons to visualize glutamate dynamics at pre- and postsynaptic microenvironments, respectively. We demonstrate that inhibition of the primarily astrocytic glutamate transporter-1 (GLT-1) slows glutamate clearance to a greater extent at presynaptic compared to postsynaptic membranes. GLT-1 expression was reduced early in a mouse model of AD, resulting in slower glutamate clearance rates at presynaptic but not postsynaptic membranes that opposed presynaptic short-term plasticity. Overall, our data demonstrate that the presynapse is particularly vulnerable to GLT-1 dysfunction and may have implications for presynaptic impairments in a variety of brain diseases.

neuroscience↗