ORCID Profile
0000-0002-7051-2090
Current Organisations
Shiraz University of Medical Sciences
,
Tehran University of Medical Sciences
,
Shahid Beheshti University
,
Florey Institute of Neuroscience and Mental Health
,
Dalhousie University
,
Johns Hopkins University
,
University of Colorado at Boulder
,
University of Pennsylvania
,
Flinders University
,
Council of Ambulance Authorities
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Publications
Effects of proNGF on Neuronal Viability, Neurite Growth and Amyloid-beta Metabolism
Publisher: Springer Science and Business Media LLC
Date: 13-08-2010
DOI: 10.1007/S12640-009-9098-X
Abstract: Alzheimer's disease (AD) is characterized pathologically by the deposition of amyloid-beta peptides (Abeta), neurofibrillary tangles, distinctive neuronal loss and neurite dystrophy. Nerve growth factor (NGF) has been suggested to be involved in the pathogenesis of AD, however, the role of its precursor (proNGF) in AD remains unknown. In this study, we investigated the effect of proNGF on neuron death, neurite growth and Abeta production, in vitro and in vivo. We found that proNGF promotes the death of different cell lines and primary neurons in culture, likely dependent on the expression of p75(NTR). We for the first time found that proNGF has an opposite role in neurite growth to that of mature NGF, retarding neurite growth in both cell lines and primary neurons. proNGF is localized to the Abeta plaques in AD mice brain, however, it had no significant effect on Abeta production in vitro and in vivo. Our findings suggest that proNGF is an important factor involving AD pathogenesis.
The impact of tau hyperphosphorylation at Ser 262 on memory and learning after global brain ischaemia in a rat model of reversible cardiac arrest
Publisher: Elsevier BV
Date: 06-2017
Early glycogen synthase kinase‐3β and protein phosphatase 2A independent tau dephosphorylation during global brain ischaemia and reperfusion following cardiac arrest and the role of the adenosine monophosphate kinase pathway
Publisher: Wiley
Date: 08-06-2016
DOI: 10.1111/EJN.13277
Reciprocal Induction Between α-Synuclein and β-Amyloid in Adult Rat Neurons
Publisher: Springer Science and Business Media LLC
Date: 19-05-2013
DOI: 10.1007/S12640-012-9330-Y
Abstract: In spite of definite roles for β-amyloid (Aβ) in familial Alzheimer's disease (AD), the cause of sporadic AD remains unknown. Amyloid senile plaques and Lewy body pathology frequently coexist in neocortical and hippoc al regions of AD and Parkinson's diseases. However, the relationship between Aβ and α-synuclein (α-Syn), the principle components in the pathological structures, in neuronal toxicity and the mechanisms of their interaction are not well studied. As Aβ and α-Syn accumulate in aging patients, the biological functions and toxicity of these polypeptides in the aging brain may be different from those in young brain. We examined the neurotoxicity influences of Aβ1-42 or α-Syn on mature neurons and the effects of Aβ1-42 or α-Syn on the production of endogenous α-Syn or Aβ1-40 reciprocally using a model of culture enriched with primary neurons from the hippoc us of adult rats. Treatment of neurons with high concentrations of Aβ1-42 or α-Syn caused significant apoptosis of neurons. Following Aβ1-42 treatment at sub apoptotic concentrations, both intra- and extra-cellular α-Syn levels were significantly increased. Reciprocally, the non-toxic levels of α-Syn treatment also increased intra- and extra-cellular Aβ1-40 levels. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002, suppressed α-Syn-induced Aβ1-40 elevation, as well as Aβ1-42-induced α-Syn elevation. Thus, high concentrations of Aβ1-42 and α-Syn exert toxic effects on mature neurons however, non-toxic concentration treatment of these polypeptides induced the production of each other reciprocally with possible involvement of PI3K pathway.
Dysregulation of Neuronal Iron Homeostasis as an Alternative Unifying Effect of Mutations Causing Familial Alzheimer's Disease.
Publisher: Frontiers Media SA
Date: 13-08-2018
Fibrillar beta-amyloid (Aβ) (1–42) elevates extracellular Aβ in cultured hippocampal neurons of adult rats
Publisher: Elsevier BV
Date: 12-2007
Alzheimer’s Disease and Cancer: When Two Monsters Cannot Be Together
Publisher: Frontiers Media SA
Date: 03-2019
Beta estradiol and norepinephrine treatment of differentiated SH-SY5Y cells enhances tau phosphorylation at (Ser396) and (Ser262) via AMPK but not mTOR signaling pathway
Publisher: Elsevier BV
Date: 04-2018
Compound C enhances tau phosphorylation at Serine396 via PI3K activation in an AMPK and rapamycin independent way in differentiated SH-SY5Y cells
Publisher: Elsevier BV
Date: 03-2018
A comparison of LKB1/AMPK/mTOR metabolic axis response to global ischaemia in brain, heart, liver and kidney in a rat model of cardiac arrest
Publisher: Springer Science and Business Media LLC
Date: 19-06-2018
Erratum: Effects of proNGF on neuronal viability, neurite growth and amyloid-beta metabolism (Neurotoxicity Research (2010) 17 (257-267) DOI: 10.1007/s12640-009-9098-x)
Publisher: Springer Science and Business Media LLC
Date: 03-09-2011
Introducing a Developed Model of Reversible Cardiac Arrest to Produce Global Brain Ischemia and Its Impact on Microtubule-Associated Protein Tau Phosphorylation at Ser396
Publisher: ClinMed International Library
Date: 28-02-2016
Tau Positive Neurons Show Marked Mitochondrial Loss and Nuclear Degradation in Alzheimer's Disease
Publisher: Bentham Science Publishers Ltd.
Date: 15-08-2018
Different fibrillar Aβ 1–42 concentrations induce adult hippocampal neurons to reenter various phases of the cell cycle
Publisher: Elsevier BV
Date: 07-2008
Oxidative Stress and Decreased Mitochondrial Superoxide Dismutase 2 and Peroxiredoxins 1 and 4 Based Mechanism of Concurrent Activation of AMPK and mTOR in Alzheimer’s Disease
Publisher: Bentham Science Publishers Ltd.
Date: 11-06-2018
Neuronal response in Alzheimer’s and Parkinson’s disease: the effect of toxic proteins on intracellular pathways
Publisher: Springer Science and Business Media LLC
Date: 23-10-2015
Modulation of Tau Phosphorylation by Oxidative Stress: Insights into the Interplay among LKB1, AMPK, and Akt Pathways in Differentiated SH-SY5Y Cells
Publisher: Authorea, Inc.
Date: 05-07-2023
Access to Ambulance Services for People with Dementia: A Comprehensive Review of Facts, Challenges, Strategies and Future Scopes
Publisher: Genesis Global Publication
Date: 23-06-2023
Development of an In Vitro Model to Evaluate the Regenerative Capacity of Adult Brain-Derived Tyrosine Hydroxylase-Expressing Dopaminergic Neurons
Publisher: Springer Science and Business Media LLC
Date: 06-03-2011
DOI: 10.1007/S11064-011-0435-0
Abstract: The loss of nigral dopaminergic (DA) neurons is the disease-defining pathological change responsible for progressive motor dysfunction in Parkinson's disease. In this study, we sought to establish a culture method for adult rat tyrosine hydroxylase (TH)-immunoreactive DA neurons. In this context, we investigated the role of fibroblast growth factor 2 (FGF2), brain-derived neurotrophic factor (BDNF), transforming growth factor-β3 (TGF-β3), glial-derived neurotrophic factor (GDNF) and dibutyryl-cyclic AMP (dbcAMP) in these cultures. Culturing in the presence of FGF2, BDNF and GDNF enhanced the survival of DA neurons by 15-fold and promoted neurite growth. In contrast, dbcAMP promoted neurite growth in all neurons but did not enhance DA cell survival. This study demonstrates that long-term cultures of DA neurons can be established from the mature rat brain and that survival and regeneration of DA neurons can be manipulated by epigenetic factors such as growth factors and intracellular cAMP pathways.
Related Organisations
Shiraz University Of Medical Sciences
Location: Iran (Islamic Republic of)
Tehran University Of Medical Sciences
Location: Iran (Islamic Republic of)
Florey Institute Of Neuroscience And Mental Health
Location: Australia
Related Funding Activities
No related grants have been discovered for Shohreh majd.