To understand the causes of dementia, Dr. Noureldein is studying oligodendrocytes, a type of glial cell that provides metabolic support to nerve cells in the brain. Specifically, his goal is to understand glia-neuron metabolic crosstalk to discover and evaluate new therapeutic targets for metabolic syndrome-associated cognitive impairment and Alzheimer’s disease and Alzheimer’s disease-related dementia. He is utilizing novel in vitro, and in vivo models combined with high throughput sequencing techniques to investigate cognitive decline and cellular communication. Additionally, Dr. Noureldein is conducting bioinformatics analysis of the microbiome (the collection of microbes in the body), single-cell RNA transcriptomic, and spatial transcriptomics data.
Dr. Noureldein’s preliminary studies indicate that oligodendrocytes play an important role in Alzheimer’s disease. He found that these support cells are metabolically impaired in Alzheimer’s disease and unable to supply energy to nerve cells in the brain. Nerve cells require a lot of energy, and when they lack energy, they cannot function properly, causing symptoms like dementia. Dr. Noureldein contends that if we can salvage oligodendrocyte function or find a way to replace their energy-supplying capacity, we could halt or possibly even reverse the damage caused by Alzheimer’s disease.
Dr. Noureldein is also well-trained in bioinformatics, an approach that uses computers to analyze and understand large amounts of biological data. Dr. Noureldein leads many of the NeuroNetwork for Emerging Therapies’ gene transcript profiling initiatives, and through bioinformatics analyses, he can show which genes are upregulated or downregulated in a particular condition. This offers insight into diseases on a molecular level and can identify new biomarkers for early diagnosis and targets for therapeutic interventions.
Other research led by Dr. Noureldein includes looking at the effect of bacteria in the gut – also known as the microbiome – on brain and nerve health. He is currently working to understand if a reduction in microbial diversity in the gut alone can alter nerve physiology and induce neuropathy and if fatty acid metabolism contributes to this process. This knowledge could provide a new therapeutic target to prevent or improve the debilitating symptoms of neuropathy, as well as inform future efforts looking at how the microbiome impacts brain health.