Biology subjects

Dickens, J. V.

Publications and source records attributed to Dickens, J. V..

6 recordsLinked to original sources

bioRxiv2026

The Georgetown Reading in Aging Neuroimaging Dataset (GRAND): Reading and multimodal MRI data in older adults

Reading is a critical skill in modern society. Most research on reading is conducted in school age children or young adults. However, acquired brain disorders often affect reading ability, and these disorders tend to occur in older adults. It is therefore critical to examine the normative distribution of reading behavior and the brain basis of reading in older adults. Here, we provide trial-wise single word and pseudoword oral reading and lexical decision data, as well as structural, functional, and diffusion-weighted MRI data from 116 neurotypical adults aged 22 to 84 years (mean = 59). Accuracy, response times, and errors are provided for corpora that are parametrically modulated in frequency, imageability, and regularity for real words and consistency of spelling-sound mapping for pseudowords. This dataset includes both minimally processed behavior (trial-wise data) and MRI data, and participant- and item-wise summary metrics and processed MRI data. These data serve both as a normative sample for reading behavior in older adults, but also as a valuable resource for identifying novel brain-behavioral relationships.

neuroscience↗

bioRxiv2025

Dissecting the sublexical route for reading: Frontal and parietal networks support learned orthography-to-phonology mappings

Oral reading relies on lexical and sublexical processes with distinct neural mechanisms. Damage within the sublexical system causes phonological alexia, a blanket diagnosis describing acquired deficits in reading unfamiliar words. Improving the precision of alexia diagnosis requires understanding the neurocognitive basis of specific reading subprocesses. This study investigated the neural correlates of sublexical reading in 64 adults with chronic left-hemisphere stroke (LHS), focusing on lesions that impair the use of learned orthography-to-phonology (OP) mappings to read new words. Participants read aloud real words and three types of pseudowords varying in the number of plausible OP mappings at the level of the orthographic body: zero mappings (0M), one mapping (1M), and multiple mappings (MM). LHS participants exhibited phonological reading deficits with an exaggerated lexicality effect compared to 71 neurotypical controls. Across both groups, pseudowords with learned OP mappings were read more accurately than those without. Voxelwise and connectome-based lesion-symptom mapping revealed that relative lexical reading deficits were associated with lateral temporal lesions, while sublexical reading deficits were associated with lesions or disconnections of the left inferior frontal (IFG), supramarginal, and pre/postcentral gyri. Applying learned OP mappings relied on anterior IFG and frontoparietal connections, while resolving multiple plausible OP mappings relied on intraparietal connections. These results underscore the role of learned mutigraphemic OP mappings in sublexical reading, and demonstrate that disruptions of different sublexical reading subprocesses result in subtly different deficit patterns. Dissecting the neurocognitive basis of reading subprocesses may improve the precision of alexia diagnosis and point to new treatments.

neuroscience↗

bioRxiv2025

Meaning for reading: The neurocognitive basis of semantic reading impairment after stroke

Diagnosis of alexia has historically focused on syndromes, such as surface alexia, which capture discrete patterns of reading deficits observed in some patients, but do not describe the breadth of reading deficits observed in practice. Aphasia research has recently shifted focus to language process impairments rather than syndromic classifications. A similar shift in focus to reading process impairments may improve our diagnostic approach to alexia. Behavioural evidence suggests that semantic processing influences reading aloud, and that semantic deficits in the context of semantic dementia underlie surface alexia. Because stroke rarely causes loss of semantic knowledge and surface alexia as a syndromic diagnosis is unusual after stroke, semantic reading deficits in stroke alexia have not previously been examined systematically. Semantic reading deficits in stroke may not relate to semantic deficits per se, but rather an inability to use semantics to support reading. Imageability, the degree to which a word brings to mind an image, is one index of semantic influences on reading. High imageability words are read more quickly by healthy persons and more accurately following brain damage. Here, we test if deficits of semantic reading after stroke, as indexed by reduced imageability effects, result from semantic or post-semantic processes. Examining nonverbal semantic processing, semantics-phonology mapping, and semantic control in a sample of 56 left-hemisphere stroke survivors, only semantics-phonology mappings predicted the reading advantage for high imageability words over low imageability words. Support vector regression voxel-based lesion symptom mapping revealed that damage along the superior temporal sulcus and underlying white matter, extending into both the middle and superior temporal gyri, reduced the advantage of high imageability over low imageability words during reading, reflecting an inability to use semantics to support reading. A similar cluster related to impairments in semantics-phonology mapping. The imageability and semantics-phonology mapping results overlapped in the left posterior superior temporal sulcus. Support vector regression connectome lesion symptom mapping revealed white matter disconnections within a broad temporoparietal network important for both phonological and semantic processing were associated with a reduction of the imageability advantage during reading. These results demonstrate that, irrespective of syndromic classification, semantic reading deficits occur in left-hemisphere stroke survivors as a result of impaired integration of semantic and phonological representations, and that the left posterior superior temporal sulcus underlies this process. Our results clarify the neurobiology of reading aloud, and support the existence of a post-semantic impairment of semantic reading in left-hemisphere stroke survivors.

neuroscience↗

bioRxiv2021

Simulated attack reveals how lesions affect network properties in post-stroke aphasia

Aphasia is one of the most prevalent cognitive syndromes caused by stroke. The rarity of premorbid imaging and heterogeneity of lesion size and extent obfuscates the links between the local effects of the lesion, global anatomical network organization, and aphasia symptoms. We applied a simulated attack approach to examine the effects of 39 stroke lesions on network topology by simulating their effects in a control sample of 36 healthy brain networks. We focused on measures of global network organization thought to support overall brain function and resilience in the whole brain and within the left hemisphere. After removing lesion volume from the network topology measures and behavioral scores (the Western Aphasia Battery Aphasia Quotient; WAB-AQ), four behavioral factor scores obtained from a neuropsychological battery, and a factor sum), we compared the behavioral variance accounted for by simulated post-stroke connectomes to that observed in the randomly permuted data. Overall, global measures of network topology in the whole brain and left hemisphere accounted for 10% variance or more of the WAB-AQ and the lexical factor score beyond lesion volume and null permutations. Streamline networks provided more reliable point estimates than FA networks. Edge weights and network efficiency were weighted most highly in predicting the WAB-AQ for FA networks. Overall, our results suggest that global network measures can provide modest statistical value predicting overall aphasia severity, but less value in predicting specific behaviors. Variability in estimates could be induced by premorbid ability, deafferentation and diaschisis, and neuroplasticity following stroke.

neuroscience↗

bioRxiv2021

Structural Disconnection of the Posterior Medial Frontal Cortex Reduces Speech Error Monitoring

Optimal performance in any task relies on the ability to detect and repair errors. The anterior cingulate cortex and the broader posterior medial frontal cortex (pMFC) are active during error processing. However, it is unclear whether damage to the pMFC impairs error monitoring. We hypothesized that successful error monitoring critically relies on connections between the pMFC and broader cortical networks involved in executive functions and the task being monitored. We tested this hypothesis in the context of speech error monitoring in people with post-stroke aphasia. Diffusion weighted images were collected in 51 adults with chronic left-hemisphere stroke and 37 age-matched control participants. Whole-brain connectomes were derived using constrained spherical deconvolution and anatomically-constrained probabilistic tractography. Support vector regressions identified white matter connections in which lost integrity in stroke survivors related to reduced error detection during confrontation naming. Lesioned connections to the bilateral pMFC were related to reduce error monitoring, including many connections to regions associated with speech production and executive function. We conclude that connections to the pMFC support error monitoring. Error monitoring in speech production is supported by the structural connectivity between the pMFC and regions involved in speech production and executive function. Interactions between pMFC and other taskrelevant processors may similarly be critical for error monitoring in other task contexts.

neuroscience↗

bioRxiv2021

Glass Half Full: Preserved Anatomical Bypasses Predict Variance in Language Functions After Stroke

The severity of post-stroke aphasia is related to damage to white matter connections. However, neural signaling can route not only through direct connections, but also along multi-step network paths. When brain networks are damaged by stroke, paths can bypass around the damage to restore communication. The shortest network paths between regions could be the most efficient routes for mediating bypasses. We examined how shortest-path bypasses after left hemisphere strokes were related to language performance. Regions within and outside of the canonical language network could be important in aphasia recovery. Therefore, we innovated methods to measure the influence of bypasses in the whole brain. Distinguishing bypasses from all residual shortest paths is difficult without pre-stroke imaging. We identified bypasses by finding shortest paths in subjects with stroke that were longer than those observed in the average network of the most reliably observed connections in age-matched controls. We tested whether features of those bypasses predicted scores in four orthogonal dimensions of language performance derived from a factor analysis of a battery of language tasks. The features were the length of each bypass in steps, and how many bypasses overlapped on each individual direct connection. We related these bypass features to language factors using grid-search cross-validated Support Vector Regression, a technique that extracts robust relationships in high-dimensional data analysis. We discovered that the length of bypasses reliably predicted variance in lexical production (R2 = .576) and auditory comprehension scores (R2 = .164). Bypass overlaps reliably predicted variance in Lexical Production scores (R2 = .247). The predictive elongation features revealed that bypass efficiency along the dorsal stream and ventral stream were most related to Lexical Production and Auditory Comprehension, respectively. Among the predictive bypass overlaps, increased bypass routing through the right hemisphere putamen was negatively related to lexical production ability.

neuroscience↗