Neurodegenerative Diseases

I– Neurodegenerative Diseases and Neuroprotection:

Motivation of research, Vision and Aim:


Investigate the neuro-protective effect of different drugs from natural or synthetic origin targeting different neurodegenerative diseases like Alzheimer’s disease, Parkinson’s disease and depression.


This research group is interested in studying the mechanism of different neurodegenerative diseases characterized by the progressive loss of structure and function of neurons. The research group is seeking to identify the causative agents and different etiologies for such disease whether genetic, environmental, secondary to other diseases, or aging. Different drugs from natural or synthetic sources are utilized for the treatment of such diseases. 

The aim is to explore the exact neuroprotective mechanism on behavioral, biochemical and molecular levels, and to compare them with reference drugs.

Previous Research Interests of the group included Hepatoprotective and antiasthmatic effects.

II - GUC Alzheimer’s Disease Unit (GADU):

Motivation, Vision and Aim:

Alzheimer’s disease is one of the most devastating neurodegenerative diseases. Unfortunately to date AD treatment is a challenge; this is due to the fact that the pathogenesis of the disease is very complicated and not well understood. Unquestionable is the fact that the pathological hallmarks of AD include accumulation of amyloid plaques, neurofibrillary tangles consisting of hyperphosphory-lated tau protein, neuroinflammation, mitochondrial dysfunction and disruption of cholinergic neurons.

Microglia, the brain innate immune cells, are activated in response to Aβ leading to neuro-inflammation in AD. Recently, two phenotypes have been described for microglia: proinflammatory classical M1 and anti-inflammatory alternative M2. Accordingly, an important strategy for AD management would be the attenuation of microglia-induced inflammation while maintaining efficient Aβ clearance. We are focusing on investigating the effect of certain drugs and natural products on microglial phenotypes and their impact on the cognitive functions and as well as Aβ level both oligomeric and fibrillar forms.

Recently, correlation between nicotinic receptors (nAChRs) dysfunction, neurodegeneration and cognitive deficits was shown in AD. nAChRs have protective role against Aβ toxicity while chronic inflammation damages cholinergic neurons and contributes to neurodegeneration. Thus, we are interested in investigating the in vivo effects of promising compounds on α -7nAChRs expression and cognitive functions in AD models. 

Mitochondrial dysfunction is believed to play a pivotal role in aging and Alzheimer’s disease (AD). Morphological and functional changes in AD mitochondria have been previously reported. Recent studies described the significant changes in proteins levels involved in mitochondrial biogenesis in AD brain tissues, demonstrating reduced mitochondrial biogenesis leading to mitochondrial dysfunction. Moreover, amyloid beta, has been shown to cause major mitochondrial dysfunction in AD. Therefore, one of our major aims is to study the mitochondrial role in AD and possible treatment modalities for the enhancement of mitochondrial functions in Alzheimer’s disease

The most important facilities that we have established in our group include different tests for the assessment of behavioral and cognitive functions, isolation of brain primary cells, phagocytic assay, different tests for measurement of mitochondrial  functions and oxidative stress, Western blotting, Real time PCR. The models that are currently used are in vivo and in vitro LPS-induced models, in vitro model for Aβ oligomers-mediated inflammation and oxidative stress.