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"Johnson, Keith"
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Phonetic Feature Encoding in Human Superior Temporal Gyrus
During speech perception, linguistic elements such as consonants and vowels are extracted from a complex acoustic speech signal. The superior temporal gyrus (STG) participates in high-order auditory processing of speech, but how it encodes phonetic information is poorly understood. We used high-density direct cortical surface recordings in humans while they listened to natural, continuous speech to reveal the STG representation of the entire English phonetic inventory. At single electrodes, we found response selectivity to distinct phonetic features. Encoding of acoustic properties was mediated by a distributed population response. Phonetic features could be directly related to tuning for spectrotemporal acoustic cues, some of which were encoded in a nonlinear fashion or by integration of multiple cues. These findings demonstrate the acoustic-phonetic representation of speech in human STG.
Journal Article
Preclinical Alzheimer disease—the challenges ahead
Pathological changes underlying Alzheimer disease (AD) begin more than 10 years before clinical presentation, and the need for early therapeutic intervention is becoming increasingly recognized. Reisa Sperling and colleagues consider challenges to such an approach—including the difficulty of defining preclinical AD, and ethical issues associated with disclosing information on AD biomarker status to healthy individuals—and discuss possible ways to overcome these hurdles.
There is growing recognition that the pathophysiological process of Alzheimer disease (AD) begins many years prior to clinically obvious symptoms, and the concept of a presymptomatic or preclinical stage of AD is becoming more widely accepted. Advances in biomarker studies have enabled detection of AD pathology
in vivo
in clinically normal older individuals. The predictive value of these biomarkers at the individual patient level, however, remains to be elucidated. The ultimate goal of identifying individuals in the preclinical stages of AD is to facilitate early intervention to delay and perhaps even prevent emergence of the clinical syndrome. A number of challenges remain to be overcome before this concept can be validated and translated into clinical practice.
Journal Article
Functional organization of human sensorimotor cortex for speech articulation
Speaking is one of the most complex actions that we perform, but nearly all of us learn to do it effortlessly. Production of fluent speech requires the precise, coordinated movement of multiple articulators (for example, the lips, jaw, tongue and larynx) over rapid time scales. Here we used high-resolution, multi-electrode cortical recordings during the production of consonant-vowel syllables to determine the organization of speech sensorimotor cortex in humans. We found speech-articulator representations that are arranged somatotopically on ventral pre- and post-central gyri, and that partially overlap at individual electrodes. These representations were coordinated temporally as sequences during syllable production. Spatial patterns of cortical activity showed an emergent, population-level representation, which was organized by phonetic features. Over tens of milliseconds, the spatial patterns transitioned between distinct representations for different consonants and vowels. These results reveal the dynamic organization of speech sensorimotor cortex during the generation of multi-articulator movements that underlies our ability to speak.
Multi-electrode cortical recordings during the production of different consonant-vowel syllables reveal distinct speech-articulator representations that are arranged somatotopically, with temporal and spatial patterns of activity across the neural population corresponding to phonetic features and dynamics.
Brain organization for speech
The act of speaking requires precisely timed coordinated movement of the lips, jaw, tongue and larynx. Edward Chang and colleagues have explored the neural basis of this precise motor control. Multi-electrode recordings in human sensorimotor cortex reveal that the region of the brain involved in speech is laid out according to a somatotopic representation of the face and vocal tract, with large populations of cells corresponding to specific phonetic features. Of particular interest is an additional laryngeal representation located at the dorsal-most end of the ventral sensorimotor cortex, apparently absent in non-human primates, that may be a feature developed uniquely for the specialized control of speech.
Journal Article
Autoradiography validation of novel tau PET tracer F-18-MK-6240 on human postmortem brain tissue
[F-18]-MK-6240, a novel tau positron emission tomography (PET) tracer recently discovered for the in vivo detection of neurofibrillary tangles, has the potential to improve diagnostic accuracy in the detection of Alzheimer disease. We have examined regional and substrate-specific binding patterns as well as possible off-target binding of this tracer on human brain tissue to advance towards its validation. We applied [F-18]-MK-6240 phosphor screen and high resolution autoradiography to postmortem samples from patients with a definite pathological diagnosis of Alzheimer disease, frontotemporal lobar degeneration-tau (Pick’s disease, progressive supranuclear palsy and corticobasal degeneration), chronic traumatic encephalopathy, frontotemporal lobar degeneration-Tar DNA-binding protein 43 (TDP-43), dementia with Lewy bodies, cerebral amyloid angiopathy and elderly controls free of pathologic changes of neurodegenerative disease. We also directly compared the binding properties of [F-18]-MK-6240 and [F-18]-AV-1451 in human tissue, and examined potential nonspecific binding of both tau tracers to monoamine oxidases (MAO) by using autoradiography in the presence of selective monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) inhibitors. Our data indicate that MK-6240 strongly binds to neurofibrillary tangles in Alzheimer disease but does not seem to bind to a significant extent to tau aggregates in non-Alzheimer tauopathies, suggesting that it may have a limited utility for the in vivo detection of these pathologies. There is no evidence of binding to lesions containing β-amyloid, α-synuclein or TDP-43. In addition, we identified MK-6240 strong off-target binding to neuromelanin and melanin-containing cells, and some weaker binding to areas of hemorrhage. These binding patterns are nearly identical to those previously reported by our group and others for [F-18]-AV-1451. Of note, [F-18]-MK-6240 and [F-18]-AV-1451 autoradiographic binding signals were only weakly displaced by competing concentrations of selective MAO-B inhibitor deprenyl but not by MAO-A inhibitor clorgyline, suggesting that MAO enzymes do not appear to be a significant binding target of any of these two tracers. Together these novel findings provide relevant insights for the correct interpretation of in vivo [F-18]-MK-6240 PET imaging.
Journal Article
Sing a song : how \Lift Every Voice and Sing\ inspired generations
Illustrations and easy-to-read text follow a family through five generations as each is inspired by the song written in 1900 to honor Abraham Lincoln. Includes author's note on the history of the song and its meaning in her family.
BOOK
Structural tract alterations predict downstream tau accumulation in amyloid-positive older individuals
Animal models of Alzheimer’s disease have suggested that tau pathology propagation, facilitated by amyloid pathology, may occur along connected pathways. To investigate these ideas in humans, we combined amyloid scans with longitudinal data on white matter connectivity, hippocampal volume, tau positron emission tomography and memory performance in 256 cognitively healthy older individuals. Lower baseline hippocampal volume was associated with increased mean diffusivity of the connecting hippocampal cingulum bundle (HCB). HCB diffusivity predicted tau accumulation in the downstream-connected posterior cingulate cortex in amyloid-positive but not in amyloid-negative individuals. Furthermore, HCB diffusivity predicted memory decline in amyloid-positive individuals with high posterior cingulate cortex tau binding. Our results provide in vivo evidence that higher amyloid pathology strengthens the association between HCB diffusivity and tau accumulation in the downstream posterior cingulate cortex and facilitates memory decline. This confirms amyloid’s crucial role in potentiating neural vulnerability and memory decline marking the onset of preclinical Alzheimer’s disease.
Journal Article