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Neuronal Injury & Repair (NIR) Laboratory

Alzheimer’s disease, metabolism hypothesis, mitochondrial dysfunction, oxidative stress...

Phosphorylated AMPK (green) in the brain
section of a rat after four weeks recovery
from 2 minutes cardiopulmonary arrest


Research Summary

The Neuronal Injury and Repair (NIR) laboratory has been focused on the effect of brain metabolic alteration on producing the hallmarks of Alzheimer’s disease. NIR lab (headship Dr. Majd) has been moved to the previous place of Parkinson’s and Alzheimer’s laboratory in 2016. Working with three systems of animal (rat) model, human brain and human neuroblastoma cell culture, this lab is focused on understanding the role of oxidative stress and mitochondrial dysfunction on Alzheimer’s disease pathology. Investigating the immediate brain strategies to modulate the function of LKB1/AMPK /mTOR pathway to maintain the energy homeostasis in response to physiological changes in cerebral circulation, or to the situations which cause the sudden disruption in energy supply, such as stroke, cardiac arrest and traumatic brain injury, is the other areas of NIR lab research.


Immuno-fluorescent staining image by Leica SP5 Confocal Microscope from right hippocampus of a human subject with Alzheimer’s disease. The neurons showed high levels of protein oxidation (DNP, red),co-localized with p-mTOR at ser2448 and p-AMPK at Thr172(green).



*For research information about Alzheimer’s disease (both in scientific and lay terms) please see the NoAlzheimer'sForMe (NOAL) website - created by the head of this lab, Dr Shohreh Majd.

Website: www.noalzheimer.com/

Facebook page: https://www.facebook.com/NoAlzheimer/


Research Projects

Identification of novel isoforms of metabolic-related proteins in the brain and their involvements in energy homeostasis in response to ischaemia, aging and Alzheimer’s pathology

As a tissue with a high metabolic rate, brain is extremely sensitive to any change in its cellular energy balance, which requires constant and rapid monitoring by the intracellular metabolic pathways. NIR lab aims to characterize two novel members of the master regulator of cell energy status, their specific roles in brain metabolism, and their involvements in brain aging as well as neuro-pathological conditions, mainly Alzheimer’s disease. The results will reveal the underlying mechanisms of the most rapid O2 sensor of the brain by identifying the structure and function of them.

The role of AMPK/mTOR signaling pathway in generating hallmarks of Alzheimer’s disease

AMPK is considered the main metabolic sensor of cells. This kinase is activated by hypoxic insults in many tissues including brain and heart with very little known about its role in Alzheimer’s disease. AMPK inhibits another intracellular pathway, mTOR, as one of its downstream targets. Upregulation of the mTOR signalling pathway is thought to play an important role in major pathological processes of Alzheimer’s disease. NIR lab investigates the contribution of AMPK and mTOR in conjunction with mitochondrial dysfunction and oxidative stress in generating AD hallmarks and the consequent cognitive decline. NIR research project will provide the first direct evidence of cellular mechanisms underlying AD- pathology due to a brain tissue oxygen alteration and also a general ischemia/reperfusion condition. We also aim to provide a possible tool to reverse or limit AD-like pathology through changing the modulating the central metabolic axis of neurons.

Selected Publications

Majd S, Power JH, Koblar SA, Grantham HJ (2017) The impact of tau hyperphosphorylation at Ser262 on memory and learning after global brain ischaemia in a rat model of reversible cardiac arrest. IBRO Reports, 2:1–13


Power JH, Barnes OL, Chegini F (2017) Lewy Bodies and the Mechanisms of Neuronal Cell Death in Parkinson's Disease and Dementia with Lewy Bodies. Brain Pathology, 27:3-12


Majd S, Power JH, Koblar SA, Grantham HJ (2016) 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. European Journal of Neuroscience, 44:1987-1997


Majd S, Power JH, Koblar SA, Grantham HJ (2016) Introducing a Developed Model of Reversible Cardiac Arrest to Produce Global Brain Ischemia and Its Impact on Microtubule-Associated Protein Tau Phosphorylation at Ser396. International Journal of Neurology and Neurotherapy, 3:1-6


Majd S, Power JH, Grantham HJ (2015) Neuronal response in Alzheimer's and Parkinson's disease: the effect of toxic proteins on intracellular pathways. BMC Neuroscience, 16:69


Majd S, Chegini F, Chataway TK, Zhou X and Gai W (2013) Reciprocal Induction Between a-synuclein and b-amyloid in Adult Rat Neurons. Neurotoxicity Research, 23(1):69-78


Dawson S, King L and Grantham H (2013) Review article: Improving the hospital clinical handover between paramedics and emergency department staff in the deteriorating patient. Emergency Medicine Australasia, 25(5):393-405


Grantham H and Narendranathan R (2012) Basic and advanced cardiac life support - what's new? Australian Family Physician, 41(6):386-390


Robinson K, Lockwood C and Grantham H (2012) First attempt success using intraosseous (IO) as an alternative to intravenous (IV) vascular access in Out of Hospital Cardiac Arrest (OHCA): a Systematic Review. JBI Library Systematic Review, 10(56)


Majd S, Smardencas A, Parish CL and Drago J (2011) Development of an In Vitro Model to Evaluate the Regenerative Capacity of Adult Brain-Derived Tyrosine Hydroxylase- Expressing Dopaminergic Neurons. Neurochemical Research, 36:967-977


Wang Y, Valadares D, Sun A, Majd S, Wang X, Zhong JH, Liu X, et al. (2010) Effects of proNGF on neuronal viability, neurite growth and amyloid-beta metabolism. Neurotoxicity Research, 17(3):257-267


Majd S, Zarifkar A, Rastegar K, Takhshid MA (2008) Different fibrillar Abeta 1-42 concentrations induce adult hippocampal neurons to reenter various phases of the cell cycle. Brain Research, 1218:224-9


Majd S, Rastegar K, Zarifkar A, Takhshid MA (2007) Fibrillar beta-amyloid (Abeta) (1-42) elevates extracellular Abeta in cultured hippocampal neurons of adult rats. Brain Research, 1185:321-7




  • Shohreh Majd, BSc (Hons), MSC, PhD (Neuroscience), GCHED (Flin)

    John Power, PhD

    Hugh Grantham, MBBS, FRACGP


    Tanushree Patel, BMS Placement Student

    Sharon Tom, BMS Placement Student

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