Mohammad Hadi Aarabi

Mr. Mohammad Hadi Aarabi

Tehran University of Medical Sciences, Tehran, Iran
orcid

Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 October 2021 in Experimental Gerontology
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Journal Article
Closed access
MFMelina Farshbafnadi
Melina Farshbafnadi
SZSara Kamali Zonouzi
Sara Kamali Zonouzi
MSMohammadmahdi Sabahi
Mohammadmahdi Sabahi
MDMahsa Dolatshahi
Mahsa Dolatshahi
MAMohammad Hadi Aarabi
Mohammad Hadi Aarabi

1 September 2020 in Molecular Neurobiology
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Journal Article
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SMSoheil Mohammadi
Soheil Mohammadi
FMFatemeh Moosaie
Fatemeh Moosaie
MAMohammad Hadi Aarabi
Mohammad Hadi Aarabi

1 October 2019 in Frontiers in Neuroendocrinology
Verified
Journal Article
Closed access
HMHossein Sanjari Moghaddam
Hossein Sanjari Moghaddam
FSFarzaneh Ghazi Sherbaf
Farzaneh Ghazi Sherbaf
MAMohammad Hadi Aarabi
Mohammad Hadi Aarabi

5 October 2018 in Human Brain Mapping
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Journal Article
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FSFarzaneh Ghazi Sherbaf
Farzaneh Ghazi Sherbaf
MAMohammad Hadi Aarabi
Mohammad Hadi Aarabi
MYMeisam Hosein Yazdi
Meisam Hosein Yazdi
MHMaryam Haghshomar
Maryam Haghshomar
Diffusion tensor imaging (DTI) has revolutionized our understanding of the neural underpinnings of alcohol teratogenesis. This technique can detect alterations in white matter in neurodevelopmental disorders, such as fetal alcohol spectrum disorder (FASD). Using Prisma guidelines, we identified 23 DTI studies conducted on individuals with prenatal alcohol exposure (PAE). These studies confirm the widespread nature of brain damage in PAE by reporting diffusivity alterations in commissural, association, and projection fibers; and in relation to increasing cognitive impairment. Reduced integrity in terms of lower fractional anisotropy (FA) and higher mean diffusivity (MD) and radial diffusivity (RD) is reported more consistently in the corpus callosum, cerebellar peduncles, cingulum, and longitudinal fasciculi connecting frontal and temporoparietal regions. Although these interesting results provide insight into FASD neuropathology, it is important to investigate the clinical diversity of this disorder for better treatment options and prediction of progression. The aim of this review is to provide a summary of different patterns of neural structure between PAE and typically developed individuals. We further discuss the association of alterations in diffusivity with demographic features and symptomatology of PAE. With the accumulated knowledge of the neural correlates of FASD presenting symptoms, a comprehensive understanding of the heterogeneity in FASD will potentially improve the disease management and will highlight the diagnostic challenges and potential areas of future research avenues, where neural markers may be beneficial.

16 April 2018 in Frontiers in Neurology
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Journal Article
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HMHossein Sanjari Moghaddam
Hossein Sanjari Moghaddam
FSFarzaneh Ghazi Sherbaf
Farzaneh Ghazi Sherbaf
MZMahtab Mojtahed Zadeh
Mahtab Mojtahed Zadeh
AAAmir Ashraf-Ganjouei
Amir Ashraf-Ganjouei
MAMohammad Hadi Aarabi
Mohammad Hadi Aarabi
The interplay between peripheral and central inflammation has a significant role in dopaminergic neural death in nigrostriatal pathway, although no direct assessment of inflammation has been performed in relation to dopaminergic neuronal loss in striatal nuclei. In this study, the correlation of neutrophil to lymphocyte ratio (NLR) as a marker of peripheral inflammation to striatal binding ratios (SBRs) of DAT SPECT images in bilateral caudate and putamen nuclei was calculated in 388 drug-naïve early PD patients [288 tremor dominant (TD), 73 postural instability and gait difficulty (PIGD), and 27 indeterminate] and 148 controls. NLR was significantly higher in PD patients than in age- and sex-matched healthy controls, and showed a negative correlation to SBR in bilateral putamen and ipsilateral caudate in all PD subjects. Among our three subgroups, only TD patients showed remarkable results. A positive association between NLR and motor severity was observed in TD subgroup. Besides, NLR could negatively predict the SBR in ipsilateral and contralateral putamen and caudate nuclei in tremulous phenotype. Nonetheless, we found no significant association between NLR and other clinical and imaging findings in PIGD and indeterminate subgroups, supporting the presence of distinct underlying pathologic mechanisms between tremor and non-tremor predominant PD at early stages of the disease.

16 June 2022 in Brain Imaging and Behavior
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Journal Article
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RRRahil Rahimi
Rahil Rahimi
MDMahsa Dolatshahi
Mahsa Dolatshahi
FAFatemeh Abbasi-Feijani
Fatemeh Abbasi-Feijani
SMSara Momtazmanesh
Sara Momtazmanesh
GCGiulia Cattarinussi
Giulia Cattarinussi
LPLorenzo Pini
Lorenzo Pini
The pathophysiology of migraine as a headache disorder is still undetermined. Diffusion tensor imaging (DTI) has significantly improved our knowledge about brain microstructure in this disease. Here, we aimed to systematically review DTI studies in migraine and survey the sources of heterogeneity by investigating diffusion parameter changes associated with clinical characteristics and migraine subtypes. Microstructural changes, as revealed by widespread alteration of diffusion metrics in white matter (WM) tracts, subcortical and cortical regions, were reported by several migraine DTI studies. Specifically, we reported changes in the corpus callosum, thalamic radiations, corona radiata, and brain stem. These alterations showed high variability across migraine cycle phases. Additionally, migraine associated with depressive/anxiety symptoms revealed significant changes in the corpus callosum, internal capsule, and superior longitudinal fasciculus. No significant WM microstructural differences were observed between migraine patients with and without aura. Overall, differences between chronic and episodic migraine showed inconsistency across studies. Migraine is associated with microstructural changes in widespread regions including thalamic radiations, corpus callosum, and brain stem. These alterations can highlight neuronal damage and neuronal plasticity mechanisms either following pain stimulations occurring in migraine cycle or as a compensatory response to pain in chronic migraine. Longitudinal studies applying advanced modalities may shed new light on the underlying microstructural changes in migraine subtypes.