About

Saud Alhusaini MD PhD is an assistant professor of Neurology at the Warren Alpert Medical School of Brown University. He earned his medical degree and a master of Neuroscience from Trinity College Dublin and completed his PhD at the Royal College of Surgeons in Ireland (RCSI). His training includes an adult neurology residency at McGill University/Montreal Neurological Institute, along with two independent fellowships: a clinical research fellowship at Yale School of Medicine and a clinical fellowship at Stanford University Medical Center. His research areas encompass essential tremor, genomics, MRI, and Parkinson's disease, contributing to the understanding of neurological disorders through extensive research and publications.

Research topics

• Neuroscience
• Genetics
• Medicine
• Biology
• Psychology
• Evolutionary biology
• Radiology
• Psychiatry

Selected publications

• Parkinson Disease <i>SNCA</i> Risk Variants Are Associated With Higher Asymmetric Putamen Dopaminergic Dysfunction

  Neurology Genetics · 2025-11-07

  articleOpen access1st authorCorresponding

  Objectives: genetic risk variants. Methods: risk variants. Results: < 0.001) and was not observed at 24-month follow-up. Discussion: risk variants, emphasizing the relevant role of neuroimaging in PD subtyping and biomarker identification.

  PublisherDOI

• Prodromal Peripheral Immune Cell Profile in Drug‐Induced Parkinsonism Relative to Parkinson's Disease

  Movement Disorders Clinical Practice · 2025-12-18

  articleOpen accessSenior authorCorresponding

  BACKGROUND: Drug-induced Parkinsonism (DIP) is a predictor of future idiopathic Parkinson's disease (PD), yet the prodromal characteristics of DIP remain unexplored. OBJECTIVES: To compare prodromal peripheral immune cell profiles in DIP and PD. METHODS: We applied independent regression models to evaluate the peripheral immune cell profiles in individuals with incident DIP (n = 108) and PD (n = 1055) relative to 20,070 healthy controls from the UK Biobank. RESULTS: Approximately 9 years before diagnosis, both DIP and PD cases exhibited elevated neutrophil counts, neutrophil-to-lymphocyte ratio (NLR), and systemic immune-inflammation index (SII). Only PD cases showed reduced lymphocyte counts. After adjusting for psychiatric comorbidities, DIP-associated peripheral immune alterations were no longer significant. CONCLUSIONS: The elevated neutrophil counts in DIP and PD suggest a shared innate immune system involvement. However, in DIP, the peripheral immune changes appear driven by psychiatric comorbidities, whereas lymphopenia may represent a distinctive prodromal biomarker of PD.

  PublisherOA PDFDOI

• Changes in Gray Matter Morphology and White Matter Microstructure Across the Adult Lifespan in People With Temporal Lobe Epilepsy.

  Open Access CRIS of the University of Bern · 2025-09-23

  articleOpen access

  Background And Objectives Temporal lobe epilepsy (TLE) is commonly associated with mesiotemporal pathology and widespread alterations of gray and white matter structures. Evidence supports a progressive condition, although the temporal evolution of TLE is poorly defined. In this ENIGMA-Epilepsy study, we aim to investigate structural alterations in gray and white matter across the adult lifespan in patients with TLE by charting both gray and white matter changes and explore the covariance of age-related alterations in both compartments.Methods Mega-analysis of parcellated T1-weighted and diffusion MRI data across 18 international sites for patients with TLE was compared against healthy controls. We combined median-age split groupwise comparisons with cross-sectional sliding age-window analyses to explore gray (cortical thickness, subcortical volume) and white matter microstructure (fractional anisotropy, mean diffusivity) age-related changes. Five-year range age windows were constructed from mean z scores of all patients. Covariance analyses examined the coupled correlations of gray and white matter lifespan curves for each region.Results We studied 769 patients with TLE and 885 healthy controls across an age range of 17-73 years. Robust (pFDR &lt; 0.05) gray matter thickness/volume decline (d &lt; -0.20) was seen across a broad cortico-subcortical territory, extending beyond the mesiotemporal lobe throughout the adult lifespan in patients with TLE. White matter changes were also widespread across multiple fiber tracts with peak effects in temporolimbic fibers in fractional anisotropy (d &lt; -0.3, pFDR &lt; 0.05) and mean diffusivity measures (d &gt; 0.3, pFDR &lt; 0.05). Changes spanned the adult time window and effects exceeded typical aging-related processes in patients at the level of cortical thickness, subcortical volume, and diffusion measures, particularly in patients older than 55 years. Covariance analyses revealed strong associations across multiple white matter tracts, subcortical structures, and cortical regions within and beyond the temporolimbic system.Discussion This study highlights that patients with TLE exhibit more pronounced and widespread gray and white matter atrophy across the lifespan. The cross-sectional nature of our study limits definitive conclusions on whether the atrophy shown is progressive but emphasizes the importance of prompt diagnosis and intervention in patients. Collectively, our results motivate future longitudinal studies to clarify consequences of drug-resistant epilepsy.

  PublisherDOI

• Peripheral Inflammation Markers in Drug-induced Parkinsonism: Findings from a Community-based Cohort (P3-5.028)

  Neurology · 2025-04-07

  articleSenior author

  To investigate the potential role of peripheral inflammation markers in drug-induced parkinsonism (DIP).

  PublisherDOI

• Changes in Gray Matter Morphology and White Matter Microstructure Across the Adult Lifespan in People With Temporal Lobe Epilepsy

  Neurology · 2025-08-22 · 3 citations

  articleOpen access

  BACKGROUND AND OBJECTIVES: Temporal lobe epilepsy (TLE) is commonly associated with mesiotemporal pathology and widespread alterations of gray and white matter structures. Evidence supports a progressive condition, although the temporal evolution of TLE is poorly defined. In this ENIGMA-Epilepsy study, we aim to investigate structural alterations in gray and white matter across the adult lifespan in patients with TLE by charting both gray and white matter changes and explore the covariance of age-related alterations in both compartments. METHODS: scores of all patients. Covariance analyses examined the coupled correlations of gray and white matter lifespan curves for each region. RESULTS: < 0.05). Changes spanned the adult time window and effects exceeded typical aging-related processes in patients at the level of cortical thickness, subcortical volume, and diffusion measures, particularly in patients older than 55 years. Covariance analyses revealed strong associations across multiple white matter tracts, subcortical structures, and cortical regions within and beyond the temporolimbic system. DISCUSSION: This study highlights that patients with TLE exhibit more pronounced and widespread gray and white matter atrophy across the lifespan. The cross-sectional nature of our study limits definitive conclusions on whether the atrophy shown is progressive but emphasizes the importance of prompt diagnosis and intervention in patients. Collectively, our results motivate future longitudinal studies to clarify consequences of drug-resistant epilepsy.

  PublisherOA PDFDOI

• Parkinson’s disease genetic risk variants are associated with larger intracranial and subcortical structure volumes in healthy and high-risk individuals

  Parkinsonism & Related Disorders · 2025-04-17

  articleSenior author
  PublisherDOI

• Case Report: Hereditary spastic paraplegia associated with monoallelic variant in the motor domain of KIF1A

  Frontiers in Human Neuroscience · 2025-05-19

  articleOpen accessSenior author

  Objectives To investigate the genetic etiology of a familial case with spastic paraplegia. Methods Neurological examination, clinical and genetic work-up, including exome sequencing (ES), followed by targeted testing, were performed to determine the underlying etiology of the patients’ phenotype. Results A 45-year-old man was initially diagnosed with spastic diplegic cerebral palsy in early childhood. He underwent multiple orthopedic interventions for lower extremities spasticity and progressive gait disturbance. His son developed similar neurological symptoms at 2-years of age. Despite unremarkable initial work-up, their relatively similar slowly progressive phenotype was suggestive of hereditary spastic paraplegia (HSP). ES was performed for the son at age 11 years, followed by cascade single testing for the father, which revealed a heterozygous (monoallelic) likely pathogenic variant [NM_001244008.2: c.947G &amp;gt; A (p.Arg316Gln); chr2-240775862] in exon 10 of the KIF1A gene. Discussion KIF1A codes for a kinesin-3 motor protein involved in neuronal axon vesicular transport. KIF1A pathogenic variants are associated with several neurological phenotypes, most commonly HSP. The rare likely pathogenic variant (p.Arg316Gln) reported here was associated with an autosomal dominant HSP with few complications.

  PublisherOA PDFDOI

• Cancer-related movement disorders: A scoping review and diagnostic approach

  Neuro-Oncology Practice · 2025-06-15

  reviewOpen accessSenior author

  Cancer-related movement disorders (CRMDs) comprise a diverse group of neurological complications of cancer. They result from varied etiologies and can be associated with compromised quality of life and poor prognosis. CRMDs can be divided into two broad categories: movement disorders resulting from cancer-related processes, such as direct tumor infiltration and paraneoplastic disease, and those that are a consequence of cancer-directed treatments, including classic therapies, such as chemotherapy and radiation therapy, novel treatments (eg immunotherapies and CAR T-Cell therapies), and various supportive treatments. A clear understanding of the breadth of CRMDs is vital, as effective management relies upon accurately identifying their underlying etiology. In this scoping review, we provide a comprehensive categorization of CRMDs based on their underlying etiology and phenomenology. Additionally, we propose a structured framework to guide the diagnostic evaluation and management of CRMDs, with the goal of facilitating timely diagnosis and, ultimately, improved patient outcomes.

  PublisherOA PDFDOI

• A – 8 Quality of Life for Patients and Caregivers with Suspected Idiopathic Normal Pressure Hydrocephalus

  Archives of Clinical Neuropsychology · 2025-09-26

  article

  Abstract Objective Idiopathic Normal Pressure Hydrocephalus (iNPH) is characterized by a triad of cognitive, urinary, and gait symptoms and can also manifest with neuropsychiatric symptoms. These symptoms may impact quality of life (QoL) and caregiver burden. We sought to identify the predictors of patient QoL and caregiver burden in individuals with suspected NPH. Method Patients (N=242, M age=74.49±8.66 years, M education=14.40±3.60, % female=37.3, % White=91.3) were evaluated in a multidisciplinary NPH clinic and self-reported information about mobility, urinary symptoms, neuropsychiatric symptoms (depression, anxiety, and apathy), and QoL. Caregivers reported on burden. Presence of cognitive impairment (binary) was determined via neuropsychological evaluation. Multivariate linear regressions examined the association between mobility, urinary, cognitive, and neuropsychiatric symptoms (predictors) and QoL and caregiver burden (outcomes) in separate models. Results Patient QoL and caregiver burden were significantly associated (r=-.492, p&amp;lt;.001). A multivariate model with mobility, urinary, cognitive, and neuropsychiatric symptoms as predictors explained 71% of the variance in QoL (R2=0.708); mobility, urinary difficulties, and apathy were significant predictors (β’s=.157-.447, p’s=.001-.046). A replicate model explained 33% of the variance in caregiving burden (R2=0.334), with patient depression and apathy predicting burden (β’s=.304-.321, p’s=.002-.017). Conclusion Patient QoL in iNPH is most associated with symptoms that tend to improve with shunting (i.e., urinary symptoms and gait changes), while caregiver burden is more closely tied to neuropsychiatric symptoms than physical symptoms. Because less is known about post-shunt changes in neuropsychiatric symptoms, despite them being predictors of caregiver burden, future studies should seek to examine treatment response for neuropsychiatric symptoms in iNPH.

  PublisherDOI

• MEK Pathway Inhibitor‐Mediated Response in BRAF V600‐Mutant Melanoma with Brain Parenchymal and Leptomeningeal Metastases

  Annals of Neurology · 2024-09-26 · 1 citations

  article1st author

  The authors have no conflicts of interest.

  PublisherDOI

Frequent coauthors

• Norman Delanty

  194 shared

• Gianpiero L. Cavalleri

  Royal College of Surgeons in Ireland

  174 shared

• Colin P. Doherty

  Trinity College Dublin

  156 shared

• Sanjay M. Sisodiya

  University College London

  152 shared

• Graeme D. Jackson

  West Virginia University

  137 shared

• Clarissa Lin Yasuda

  Universidade Estadual de Campinas (UNICAMP)

  134 shared

• Fernando Cendes

  Brazilian Institute of Neuroscience and Neurotechnology

  126 shared

• Mira Semmelroch

  Florey Institute of Neuroscience and Mental Health

  122 shared

Education

• M.D.

  Trinity College Dublin

• M.S., Neuroscience

  Trinity College Dublin

• Ph.D.

  Royal College of Surgeons in Ireland (RCSI)