The predominant theories of developmental dyslexia view the underlying disorder as arising from dysfunction in the cerebral cortex. Similarly, efforts to understand the neural basis of reading development have focused largely upon the cerebral cortex. However, because predominant theories of dyslexia do not capture its full behavioral phenotype, there has been continued consideration of alternative perspectives on the neural substrates of reading development and dyslexia. The current proposal evaluates one such alternative theory, the ?cerebellar deficit hypothesis? proposed by Nicolson and colleagues. We propose a variant of this hypothesis that arose from a meta-analytic review of the reading literature, the CDH* model. In the CDH* model, a fusiform-parietal-frontal (dorsal) pathway supports the decoding of unfamiliar printed words, with cerebellar connectivity into this pathway improving the representational similarity between the parietal and frontal nodes. This increases the likelihood that a given item will be decoded successfully, and thus induce orthographic learning. A ventrally connected cerebellar-cerebral circuit involving a fusiform-temporal-frontal pathway is proposed to play an assistive role, by providing lexical-semantic constraints when decoding demands are high. We investigate the CDH* model across three aims involving functional magnetic resonance imaging and behavioral studies in adult subjects, and the use of orthographic learning protocols to study reading development from an item-based (rather than stage-based) perspective.
In Aim 1, we study adults reading words printed in a newly learned artificial orthography, and test for predicted relationships between cerebellar-cerebral connectivity, representational similarity, decoding success, and orthographic learning, and the impact of phonological demands on these relationships.
In Aim 2, we will test whether individuals with and without dyslexia have differences in cerebellar- cerebral connectivity that can account for group differences in effective connectivity, decoding ability, and orthographic learning.
In Aim 3, we will use the lesion method to test for a causal relationship between acquired cerebellar damage and impairments in decoding and orthographic learning. By advancing current understanding of how the cerebellum ? one of the brain's core learning systems ? interfaces with a cerebral reading network, the work has the potential to widely influence theories of reading development and dyslexia.

Public Health Relevance

The current proposal evaluates an alternative theory of the neural substrates of reading development and dyslexia, the ?cerebellar deficit hypothesis?. By advancing current understanding of how the cerebellum ? one of the brain's core learning systems ? interfaces with a cerebral reading network, the work has the potential to widely influence theories of reading development and dyslexia.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD096738-02
Application #
10017309
Study Section
Language and Communication Study Section (LCOM)
Program Officer
Miller, Brett
Project Start
2019-09-12
Project End
2024-07-31
Budget Start
2020-08-01
Budget End
2021-07-31
Support Year
2
Fiscal Year
2020
Total Cost
Indirect Cost
Name
University of Pittsburgh
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
004514360
City
Pittsburgh
State
PA
Country
United States
Zip Code
15260