The minimal clinically important difference of two multifaceted fatigue evaluation questionnaires in chronic stroke.

PURPOSE: This research sought to ascertain the Minimal Clinically Important Difference (MCID) and Robust Clinically Important Difference (RCID) of the Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF) and Chalder Fatigue Questionnaire-11 (CFQ-11) as two important concepts for the clinical interpretation of the results in chronic post-stroke population. METHODS: A total of 128 subjects with chronic post-stroke completed the MFSI-SF and CFQ-11 before and after six weeks of intervention. The MCIDs were derived using both anchor- and distribution-based methods; however, only anchor-based methods were used to estimate RCIDs. RESULTS: Anchor-based MCIDs for MFSI-SF and CFQ-11 were in the range of -5 to -6.28 and -2 to -4.56, respectively. Distribution-based MCIDs in MFSI-SF and CFQ-11 were calculated in the range of -4.17 to -24.05 and -1.72 to -7.68, respectively. RCID ranges of -10 to -15 were obtained for the MFSI-SF and -6 to -7.33 for the CFQ-11. CONCLUSION: These findings may have implications for clinical experts in the clinical interpretation of fatigue changes observed in MFSI-SF and CFQ-11 in individuals with chronic stroke.

Early Auditory Temporal Processing Deficit in Children with Autism Spectrum Disorder: The Research Domain Criteria Framework.

Altered sensory processing especially in the auditory system is considered a typical observation in children with autism spectrum disorder (ASD). Auditory temporal processing is known to be impaired in ASD children. Although research suggests that auditory temporal processing abnormalities could be responsible for the core aspects of ASD, few studies have examined early time processing and their results have been conflicting. The present event-related potential (ERP) study investigated the early neural responses to duration and inter-stimulus interval (ISI) deviants in nonspeech contexts in children with ASD and a control group of typically developing (TD) children matched in terms of age and IQ. A passive auditory oddball paradigm was employed to elicit the mismatch negativity (MMN) for change detection considering both the duration and ISI-based stimulus. The MMN results showed that the ASD group had a relatively diminished amplitude and significant delayed latency in response to duration deviants. The findings are finally discussed in terms of hyper-hyposensitivity of auditory processing and the fact that the observed patterns may potentially act as risk factors for ASD development within the research domain criteria (RDoC) framework.

The role of CART peptide in learning and memory: A potential therapeutic target in memory-related disorders.

Cocaine and amphetamine-regulated transcript (CART) mRNA and peptide are vastly expressed in both cortical and subcortical brain areas and are involved in critical cognitive functions. CART peptide (CARTp), described in reward-related brain structures, regulates drug-induced learning and memory, and its role appears specific to psychostimulants. However, many other drugs of abuse, such as alcohol, opiates, nicotine, and caffeine, have been shown to alter the expression levels of CART mRNA and peptides in brain structures directly or indirectly associated with learning and memory processes. However, the number of studies demonstrating the contribution of CARTp in learning and memory is still minimal. Notably, the exact cellular and molecular mechanisms underlying CARTp effects are still unknown. The discoveries that CARTp effects are mediated through a putative G-protein coupled receptor and activation of cellular signaling cascades via NMDA receptor-coupled ERK have enhanced our knowledge about the action of this neuropeptide and allowed us to comprehend better CARTp exact cellular/molecular mechanisms that could mediate drug-induced changes in learning and memory functions. Unfortunately, these efforts have been impeded by the lack of suitable and specific CARTp receptor antagonists. In this review, following a short introduction about CARTp, we report on current knowledge about CART's roles in learning and memory processes and its recently described role in memory-related neurological disorders. We will also discuss the importance of further investigating how CARTp interacts with its receptor(s) and other neurotransmitter systems to influence learning and memory functions. This topic is sure to intrigue and motivate further exploration in the field of neuroscience.

Minimal and robust clinically important differences for patient-reported outcome measures of fatigue in chronic stroke survivors after fatigue rehabilitation.

PURPOSE: The minimal and robust clinically important difference (MCID and/or RCID) are essential in assessing the clinical significance of multidimensional fatigue inventory-20 and checklist of individual strength-fatigue subscale questionnaires changes scores. This is the first study to determine the MCID and RCID of these questionnaires in chronic stroke survivors. MATERIALS AND METHODS: A total of 125 participants in an observational cohort study completed MFI-20 and CIS-fs before and after receiving multidisciplinary rehabilitation (cognitive behavioral therapy, graded exercise and adaptive pacing therapy). Anchor-based MCIDs and RCIDs were calculated using the mean change, the mean difference and the receiver operating characteristics methods. To evaluate the accordance between of distribution-based MCIDs (1 SD, ½ SD, SEM, 1.96 SEM and MDC values) with anchored values, the accuracy, sensitivity, specificity and Youden's index were calculated. RESULTS: The anchored MCIDs were between -5 to -7.33 for MFI-20 and -4.87 to -5.40 for CIS-fs. The anchored RCIDs ranged from -5 to -13.88 and -6 to -9.88 for MFI-20 and CIS-fs, respectively. The values of ½ SD and SEM for CIS-fs were consistent with anchored RCIDs. CONCLUSIONS: The estimated MCIDs and RCIDs of MFI-20 and CIS-fs can help researchers and clinicians interpret their chronic stroke patient data.

The Multidimensional Fatigue Inventory-20 (MFI-20) And Checklist Individual Strength-20 (CIS-20) Measures Are Two Important And Valid Instruments For Measuring Fatigue In Patients With Chronic Stroke.The Identified Minimal Clinically Important Differences (MCID) And Robust Clinically Important Difference In The Current Study Can Assist Clinicians In The Clinical Interpretation Of Fatigue Changes Observed In MFI-20 And CIS-20 Scores.The MCID Obtained In This Study Can Be Useful In Determining The Proportion Of Patients Who Benefit From Fatigue Treatment In Stroke Rehabilitation.

Sodium Phenylbutyrate and Tauroursodeoxycholic Acid: A Story of Hope Turned to Disappointment in Amyotrophic Lateral Sclerosis Treatment.

The absence of a definitive cure for amyotrophic lateral sclerosis (ALS) emphasizes the crucial need to explore new and improved treatment approaches for this fatal, progressive, and disabling neurodegenerative disorder. As at the end of 2023, five treatments - riluzole, edaravone, dextromethorphan hydrobromide + quinidine sulfate (DHQ), tofersen, and sodium phenylbutyrate-tauroursodeoxycholic acid (PB-TUDCA) - were FDA approved for the treatment of patients with ALS. Among them PB-TUDCA has been shown to impact DNA processing impairments, mitochondria dysfunction, endoplasmic reticulum stress, oxidative stress, and pathologic folded protein agglomeration defects, which have been associated with ALS pathophysiology. The Phase 2 CENTAUR trial demonstrated significant impact of PB-TUDCA on the ALS Functional Rating Scale-Revised (ALSFRS-R) risk of death, hospitalization, and the need for tracheostomy or permanent assisted ventilation in patients with ALS based on post hoc analyses. More recently, contrasting with the CENTAUR trial results, results from the Phase 3 PHOENIX trial (NCT05021536) showed no change in ALSFRS-R total score at 48 weeks. Consequently, the sponsor company initiated the process with the US FDA and Health Canada to voluntarily withdraw the marketing authorizations for PB-TUDCA. In the present article, we review ALS pathophysiology, with a focus on PB-TUDCA's proposed mechanisms of action and recent clinical trial results and discuss the implications of conflicting trial data for ALS and other neurological disorders.

Unraveling the potential of CD8, CD68, and VISTA as diagnostic and prognostic markers in patients with pancreatic ductal adenocarcinoma.

Introduction: Pancreatic cancer is a truculent disease with limited treatment options and a grim prognosis. Immunotherapy has shown promise in treating various types of cancer, but its effectiveness in pancreatic cancer has been lacking. As a result, it is crucial to identify markers associated with immunological pathways in order to improve the treatment outcomes for this deadly cancer. The purpose of this study was to investigate the diagnostic and prognostic significance of three markers, CD8, CD68, and VISTA, in pancreatic ductal adenocarcinoma (PDAC), the most common subtype of pancreatic cancer. Methods: We analyzed gene expression data from Gene Expression Omnibus (GEO) database using bioinformatics tools. We also utilized the STRING online tool and Funrich software to study the protein-protein interactions and transcription factors associated with CD8, CD68, and VISTA. In addition, tissue microarray (TMA) and immunohistochemistry (IHC) staining were performed on 228 samples of PDAC tissue and 10 samples of normal pancreatic tissue to assess the expression levels of the markers. We then correlated these expression levels with the clinicopathological characteristics of the patients and evaluated their survival rates. Results: The analysis of the GEO data revealed slightly elevated levels of VISTA in PDAC samples compared to normal tissues. However, there was a significant increase in CD68 expression and a notable reduction in CD8A expression in pancreatic cancer. Further investigation identified potential protein-protein interactions and transcription factors associated with these markers. The IHC staining of PDAC tissue samples showed an increased expression of VISTA, CD68, and CD8A in pancreatic cancer tissues. Moreover, we found correlations between the expression levels of these markers and certain clinicopathological features of the patients. Additionally, the survival analysis revealed that high expression of CD8 was associated with better disease-specific survival and progression-free survival in PDAC patients. Conclusion: These findings highlight the potential of CD8, CD68, and VISTA as diagnostic and prognostic indicators in PDAC.

Intracerebroventricular Cutibacterium acnes Generates Manifestations of Alzheimer's Disease-like Pathology in the Rat Hippocampus.

The infection hypothesis is a new causative explanation for Alzheimer's disease (AD). In recent decades, various species of bacterial pathogens have been distinguished in the autopsy of Alzheimer's patients; however, the mechanism of bacterial contribution to AD pathology is still unknown. To explore the hypothesis, Cutibacterium acnes (C. acnes) was selected, and effects of its intracerebroventricular (ICV) inoculation in rats was evaluated. The results revealed that C. acnes causes memory impairment, which might be a consequence of upregulated Amyloid ß (Aß) deposits in the hippocampus; Aß aggregates are co-localized with C. acnes colonies. The key point of our hypothesis is that the activation of the innate immune system by C. acnes through the TLR2/NF-κB/NLRP3 signaling pathway, eventually leads to increased neuroinflammation, which might be resulted from microgliosis and astrogliosis. Neuroinflammation increases oxidative stress and cell apoptosis. Overall, the obtained results of this study support our hypothesis that brain exposure to C. acnes prompted neuroinflammation with similar AD-like pathology.

Neurodegeneration with Brain Iron Accumulation Disorders and Retinal Neurovascular Structure.

BACKGROUND: The unique neurovascular structure of the retina has provided an opportunity to observe brain pathology in many neurological disorders. However, such studies on neurodegeneration with brain iron accumulation (NBIA) disorders are lacking. OBJECTIVES: To investigate NBIA's neurological and ophthalmological manifestations. METHODS: This cross-sectional study was conducted on genetically confirmed NBIA patients and an age-gender-matched control group. The thickness of retinal layers, central choroidal thickness (CCT), and capillary plexus densities were measured by spectral domain-optical coherence tomography (SD-OCT) and OCT angiography, respectively. The patients also underwent funduscopy, electroretinography (ERG), visual evoked potential (VEP), and neurological examination (Pantothenate-Kinase Associated Neurodegeneration-Disease Rating Scale [PKAN-DRS]). The generalized estimating equation model was used to consider inter-eye correlations. RESULTS: Seventy-four patients' and 80 controls' eyes were analyzed. Patients had significantly decreased visual acuity, reduced inner or outer sectors of almost all evaluated layers, increased CCT, and decreased vessel densities, with abnormal VEP and ERG in 32.4% and 45.9%, respectively. There were correlations between visual acuity and temporal peripapillary nerve fiber layer (positive) and between PKAN-DRS score and disease duration (negative), and scotopic b-wave amplitudes (positive). When considering only the PKAN eyes, ONL was among the significantly decreased retinal layers, with no differences in retinal vessel densities. Evidence of pachychoroid was only seen in patients with Kufor Rakeb syndrome. CONCLUSION: Observing pathologic structural and functional neurovascular changes in NBIA patients may provide an opportunity to elucidate the underlying mechanisms and differential retinal biomarkers in NBIA subtypes in further investigations. © 2023 International Parkinson and Movement Disorder Society.

Dynamic causal modeling of reorganization of memory and language networks in temporal lobe epilepsy.

OBJECTIVE: To evaluate the alterations of language and memory functions using dynamic causal modeling, in order to identify the epileptogenic hemisphere in temporal lobe epilepsy (TLE). METHODS: Twenty-two patients with left TLE and 13 patients with right TLE underwent functional magnetic resonance imaging (fMRI) during four memory and four language mapping tasks. Dynamic causal modeling (DCM) was employed on fMRI data to examine effective directional connectivity in memory and language networks and the alterations in people with TLE compared to healthy individuals. RESULTS: DCM analysis suggested that TLE can influence the memory network more widely compared to the language network. For memory mapping, it demonstrated overall hyperconnectivity from the left hemisphere to the other cranial regions in the picture encoding, and from the right hemisphere to the other cranial regions in the word encoding tasks. On the contrary, overall hypoconnectivity was seen from the brain hemisphere contralateral to the seizure onset in the retrieval tasks. DCM analysis further manifested hypoconnectivity between the brain's hemispheres in the language network in patients with TLE compared to controls. The CANTAB® neuropsychological test revealed a negative correlation for the left TLE and a positive correlation for the right TLE cohorts for the connections extracted by DCM that were significantly different between the left and right TLE cohorts. INTERPRETATION: In this study, dynamic causal modeling evidenced the reorganization of language and memory networks in TLE that can be used for a better understanding of the effects of TLE on the brain's cognitive functions.

Aquaporin 4 beyond a water channel; participation in motor, sensory, cognitive and psychological performances, a comprehensive review.

Aquaporin 4 (AQP4) is a protein highly expressed in the central nervous system (CNS) and peripheral nervous system (PNS) as well as various other organs, whose different sites of action indicate its importance in various functions. AQP4 has a variety of essential roles beyond water homeostasis. In this article, we have for the first time summarized different roles of AQP4 in motor and sensory functions, besides cognitive and psychological performances, and most importantly, possible physiological mechanisms by which AQP4 can exert its effects. Furthermore, we demonstrated that AQP4 participates in pathology of different neurological disorders, various effects depending on the disease type. Since neurological diseases involve a spectrum of dysfunctions and due to the difficulty of obtaining a treatment that can simultaneously affect these deficits, it is therefore suggested that future studies consider the role of this protein in different functional impairments related to neurological disorders simultaneously or separately by targeting AQP4 expression and/or polarity modulation.

Persian version of the Chalder Fatigue Questionnaire and Multidimensional Fatigue Symptom Inventory-Short Form: psychometric properties in Iranian chronic stroke survivors.

BACKGROUND: Post-stroke fatigue is a disturbing condition with various physical and psychological facets, which needs to be assessed by meaningful and psychometrically valid and reliable tools. The Chalder Fatigue Questionnaire (CFQ) and Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF) have been designed to assess diverse dimensions of fatigue. OBJECTIVES: The present study aimed to investigate the psychometric properties of the CFQ and MFSI-SF in people with chronic stroke. METHODS: Both measures were translated according to forward-backward standard protocol. This cross-sectional study was conducted with 130 first-time stroke survivors. The multidimensional fatigue inventory, checklist individual strength, fatigue assessment scale, fatigue subscale of profiles of mood state, fatigue severity scale, visual analogue scale-fatigue, beck anxiety inventory, center for epidemiologic studies of depression scale, and 36-item short-form health survey were administered in addition to the CFQ and MFSI-SF. Reliability, precision, known-groups validity, and convergent validity were examined for the CFQ and MFSI-SF. RESULTS: The results showed an acceptable (Cronbach's alpha = 0.81-0.97) internal consistency and test-retest reliability (intra-class correlation = 0.75-0.97). The CFQ and MFSI-SF revealed good ability (P < 0.001) to differentiate chronic stroke survivors with different disability levels. Significant high correlation (P = -0.61-0.87) was found between CFQ and MFSI-SF and other fatigue scales. CONCLUSIONS: The results of this study showed that the CFQ and MFSI-SF have high reliability and validity for chronic stroke survivors.

Inhibition of autotaxin alleviates pathological features of hepatic encephalopathy at the level of gut-liver-brain axis: an experimental and bioinformatic study.

There is accumulating evidence that the circulatory levels of autotaxin (ATX) and lysophosphatidic acid (LPA) are increased in patients with severe liver disease. However, the potential role of the ATX-LPA axis in hepatic encephalopathy (HE) remains unclear. Our study aimed to investigate the role of the ATX-LPA signaling pathway in mice with thioacetamide (TAA) induced acute HE. To show the role of the ATX-LPA axis in the context of HE, we first measured the involvement of ATX-LPA in the pathogenesis of TAA-induced acute HE. Then, we compared the potential effects of ATX inhibitor (HA130) on astrocyte responses at in vitro and gut-liver-brain axis at in vivo levels. The inflammatory chemokine (C-C motif) ligand 3 was significantly increased in the hyperammonemic condition and could be prevented by ATX inhibition in astrocytes at in vitro level. Further statistical tests revealed that plasma and tissue pro-inflammatory cytokines were inhibited by HA130 in mice. Furthermore, the stage of HE was significantly improved by HA130. The most surprising result was that HA130 alleviated immune infiltrating cells in the liver and intestine and decreased mucus-secreting cells in the intestine. Further analysis showed that the levels of liver enzymes in serum were significantly decreased in response to ATX inhibition. Surprisingly, our data indicated that HA130 could recover permeabilization of the blood-brain barrier, neuroinflammation, and recognition memory. Besides that, we found that the changes of Interleukin-1 (IL-1) and aquaporin-4 (AQP4) in HE might have a connection with the glymphatic system based on bioinformatics analyses. Taken together, our data showed that the ATX-LPA axis contributes to the pathogenesis of HE and that inhibition of ATX improves HE.

The role of neurotransmitters in glioblastoma multiforme-associated seizures.

GBM, or glioblastoma multiforme, is a brain tumor that poses a great threat to both children and adults, being the primary cause of death related to brain tumors. GBM is often associated with epilepsy, which can be debilitating. Seizures and the development of epilepsy are the primary symptoms that have a severe impact on the quality of life for GBM patients. It is increasingly apparent that the nervous system plays an essential role in the tumor microenvironment for all cancer types, including GBM. In recent years, there has been a growing understanding of how neurotransmitters control the progression of gliomas. Evidence suggests that neurotransmitters and neuromodulators found in the tumor microenvironment play crucial roles in the excitability, proliferation, quiescence, and differentiation of neurons, glial cells, and neural stem cells. The involvement of neurotransmitters appears to play a significant role in various stages of GBM. In this review, the focus is on presenting updated knowledge and emerging ideas regarding the interplay between neurotransmitters and neuromodulators, such as glutamate, GABA, norepinephrine, dopamine, serotonin, adenosine, and their relationship with GBM and the seizures induced by this condition. The review aims to explore the current understanding and provide new insights into the complex interactions between these neurotransmitters and neuromodulators in the context of GBM-related seizures.

Cancer cells same as zombies reprogram normal cells via the secreted microenvironment.

The cancer microenvironment plays a crucial role in promoting metastasis and malignancy even in normal cells. In the present study, the effect of acidic and conditioned media of cancer cells (MDA-MB-231), separately and in combination, was studied for the first time on the cell death mechanisms and DNA methylation of normal fibroblasts (NIH/3T3). Cell survival of conditioned media was rescued by the addition of acidic media to conditioned media, as shown by the results. Cell metabolic activity is deviated in a direction other than the Krebs cycle by acidic media The mitochondrial metabolic activity of all groups was enhanced over time, except for acidic media. Unlike the highest amount of ROS in conditioned media, its level decreased to the level of acidic media in the combination group. Furthermore, cells were deviated towards autophagy, rather than apoptosis, by the addition of acidic media to the conditioned media, unlike the conditioned media. Global DNA methylation analysis revealed significantly higher DNA hypomethylation in acidic media than in normal and combination media. Not only were cells treated with conditioned media rescued by acidic media, but also DNA hypomethylation and apoptosis in the combination group were decreased through epigenetic modifications. The acidic and conditioned media produced by cancer cells can remotely activate malignant signaling pathways, much like zombies, which can cause metabolic and epigenetic changes in normal cells.

Focusing on the locus of the breakdown for treatment of anomia: a pilot study.

The primary goal of this study was to evaluate the treatment effects of semantic feature analysis (SFA) and phonological components analysis (PCA) on word retrieval processing in persons with aphasia (PWAs). After identifying the locus of the breakdown in lexical retrieval processing, 15 monolingual native Persian speakers with aphasia were divided into two groups. After three naming trials, participants with dominant semantic deficits received SFA, and participants with primary phonological deficits were provided with PCA three times a week for eight weeks. Both approaches improved participants' naming and performance on language tests, including spontaneous speech, repetition, comprehension, and semantic processing. However, the correct naming of treated and untreated items was higher in mild-to-moderate participants, with mostly circumlocution and semantic paraphasias in the SFA group. The same holds for mild-to-moderate participants with mostly phonemic paraphasia who received PCA therapy. Moreover, the results showed that participants' baseline naming performance and semantic abilities could be associated with the treatment outcomes. Although limited by a lack of a control group, this study provided evidence supporting the possible benefits of focusing on the locus of the breakdown for treating anomia through SFA and PCA approaches, specifically in participants with mild to moderate aphasia. However, for those with severe aphasia, the treatment choice may not be as straightforward because several variables are likely to contribute to this population's word-finding difficulties. Replication with larger, well-stratified samples, use of a within-subjects alternating treatment design and consideration of treatments' long-term effects are required to better ascertain the effects of focusing on the locus of breakdown for treatment of anomia.

High and Low-Frequency Stimulation Effect on Epileptiform Activity in Brain Slices.

Background: Neurostimulation is one of the new therapeutic approaches in patients with drug-resistant epilepsy, and despite its high efficiency, its mechanism of action is still unclear. On the one hand, electrical stimulation in the human brain is immoral; on the other hand, the creation of the epilepsy model in laboratory animals affects the entire brain network. As a result, one of the ways to achieve the neurostimulation mechanism is to use epileptiform activity models In vitro. In vitro models, by accessing the local network from the whole brain, we can understand the mechanisms of action of neurostimulation. Methods: A literature search using scientific databases including PubMed, Google Scholar, and Scopus, using "Neurostimulation" and "epileptiform activity" combined with "high-frequency stimulation", " low-frequency stimulation ", and "brain slices" as keywords were conducted, related concepts to the topic gathered and are used in this paper. Results: Electrical stimulation causes neuronal depolarization and the release of GABAA, which inhibits neuronal firing. Also, electrical stimulation inhibits the nervous tissue downstream of the stimulation site by preventing the passage of nervous activity from the upstream to the downstream of the axon. Conclusion: Neurostimulation techniques consisting of LFS and HFS have a potential role in treating epileptiform activity, with some studies having positive results. Further investigations with larger sample sizes and standardized outcome measures can be conducted to validate the results of previous studies.

Neurostimulation as a Putative Method for the Treatment of Drug-resistant Epilepsy in Patient and Animal Models of Epilepsy.

A patient with epilepsy was shown to have neurobiological, psychological, cognitive, and social issues as a result of recurring seizures, which is regarded as a chronic brain disease. However, despite numerous drug treatments, approximately, 30%-40% of all patients are resistant to antiepileptic drugs. Therefore, newer therapeutic modalities are introduced into clinical practice which involve neurostimulation and direct stimulation of the brain. Hence, we review published literature on vagus nerve stimulation, trigeminal nerve stimulation, applying responsive stimulation systems, and deep brain stimulation (DBS) in animals and epileptic patient with an emphasis on drug-resistant epilepsy.

Verbal Working Memory-Balance program training alters the left fusiform gyrus resting-state functional connectivity: A randomized clinical trial study on children with dyslexia.

Sufficient activation of the left fusiform gyrus is important in reading ability acquisition due to its role in reading and naming, working memory (WM), and balance tasks. Recently, a newly-designed training program, Verbal Working Memory-Balance (VWM-B), has been evaluated on children with dyslexia, and its positive effects were shown on reading ability, WM capacity, and postural control. In the present study, we aimed to estimate the functional connectivity alterations of the left fusiform gyrus following training by the VWM-B. Before and after 15 sessions of training, the fMRI and other tools data were collected on a sample of children with dyslexia, who were allocated into two control and experiment groups. Data analyses showed the increased functional connectivity of the left fusiform gyrus between the left anterior temporal fusiform cortex, left and right Crus II regions of the cerebellum, and the left middle frontal gyrus. Moreover, VWM-B training significantly improved the reading and naming ability, WM capacity, and postural control of participants in the experiment group in comparison to the control. The current study findings emphasize the critical role of the left fusiform gyrus in reading ability. Moreover, it provides evidence to support the existence of cerebellar deficits in dyslexia.