Biology subjects

Spinazzi, E.

Publications and source records attributed to Spinazzi, E..

3 recordsLinked to original sources

bioRxiv2026

A Fully Endovascular Neural Interface

Electrical stimulation of neural circuits is expanding therapeutic strategies to modulate brain, autonomic, and immune functions. Devices delivered endovascularly offer a less invasive alternative to conventional implanted electrodes, while delivering spatio-temporal specificity superior to noninvasive techniques. We demonstrate a fully endovascular sub-1-mm3 implant, utilizing ultrasound for wireless power delivery and data telemetry in a fashion invariant to device orientation. The implant consists of piezoelectric transducers, an energy storage capacitor, an application-specific integrated circuit, and electrodes packaged on a 7-{micro}m-thick polyimide scaffold. The implant can be delivered through a microcatheter in a manner analogous to conventional neurovascular stents, and self-expands upon deployment to appose the vessel walls. We demonstrate intravascular stimulation of the autonomic nervous system from the carotid artery, achieving modulation of blood pressure in rabbits. This approach establishes a broadly applicable platform for neural interfaces enabling both stimulation and recording.

neuroscience↗

bioRxiv2024

Stable, chronic in-vivo recordings from a fully wireless subdural-contained 65,536-electrode brain-computer interface device

Minimally invasive, high-bandwidth brain-computer-interface (BCI) devices can revolutionize human applications. With orders-of-magnitude improvements in volumetric efficiency over other BCI technologies, we developed a 50-m-thick, mechanically flexible micro-electrocorticography (ECoG) BCI, integrating a 256x256 array of electrodes, signal processing, data telemetry, and wireless powering on a single complementary metal-oxide-semiconductor (CMOS) substrate containing 65,536 recording channels, from which we can simultaneously record a selectable subset of up to 1024 channels at a given time. Fully implanted below the dura, our chip is wirelessly powered, communicating bi-directionally with an external relay station outside the body. We demonstrated chronic, reliable recordings for up to two weeks in pigs and up to two months in behaving non-human primates from somatosensory, motor, and visual cortices, decoding brain signals at high spatiotemporal resolution.

neuroscience↗

bioRxiv2020

Neuroinflammation characterizes the earliest changes in Alzheimer's disease pathology and associated subjective cognitive impairment in adult hydrocephalus biopsies

In an effort to better characterize the transcriptomic changes that accompany early Alzheimers disease (AD) pathology in living patients and correlate with contemporaneous cognitive data, we performed RNA-seq on 106 cortical biopsies that were taken during shunt placement for adult onset hydrocephalus with varying degrees of comorbid AD pathology. A restricted set of genes correlate with AD pathology in these biopsies, and co-expression network analysis demonstrates an evolution from microglial homeostasis to a disease-associated microglial phenotype in conjunction with increasing AD pathologic burden, along with a subset of additional astrocytic and neuronal genes that accompany these changes. Further analysis demonstrates that these correlations are driven by patients that report mild cognitive symptoms, despite similar levels of {beta}-amyloid and tau pathology in comparison to patients who report no cognitive symptoms. Interestingly, downregulation of homeostatic genes and upregulation of disease-associated genes also correlate with microglial plaque invasion and an activated microglial morphology, and this change is not sensitive to cognitive status, suggesting that an initial microglial response to AD pathology is eventually maladaptive. Taken together, these findings highlight a restricted set of microglial and non-microglial genes and suggest that early AD pathology is largely characterized by a loss of homeostatic genes and an activated microglial phenotype that continues to evolve in conjunction with accumulating AD pathology in the setting of subjective cognitive decline.

neuroscience↗