- Head of laboratory
- Scientific Staff
- Technician and administration staff
- PhD Students
- Research profile
- Current activities
- Selected publications
Life experiences and environmental conditions are strong determinants of brain health in humans. Long-term exposure to adverse conditions, such as traumatic experiences or nutritional insults can not only lead to brain diseases in the exposed individuals but such disease susceptibilities may also be transmitted to their offspring. Two important molecular pathways connect environmental exposures to brain disorders; 1) epigenetic factors, such as non-coding RNAs (ncRNAs), and 2) metabolic factors. Notably, our previous research showed a causal role for ncRNAs in intergenerational transmission of neuropsychiatric disease risk after early life trauma and a potential role for metabolic pathways in mediating this transmission. Jawaid lab now aims to further disset the liaison between ncRNAs and lipid molecules in neuropsychiatric sequelae of early life trauma; and investigate how metabolism can be manipulated to counter its neuropsychiatric manifestations across generations.
Our current projects include in vitro, ex vivo, and in vivo studies on:
– Role of metabolic factors in epigenetic propagation of childhood trauma
– Metabolic and epigenetic regulation of microglial phagocytosis in neurodegeneration
– Targeting metabolism against pathological protein aggregation in neurodegeneration
– Molecular cascades involved in post-COVID ‘Brain fog’
Jawaid A, Jehle K, Manusy IM. Impact of parental exposures on offspring health in humans. Trends in Genetics 2020. doi: 10.1016/j.tig.2020.10.006.
Jawaid A. Protecting older adults during social distancing. Science. 2020;386:6487.
Jawaid A, Khan RA, Kremer EA, Polymenidou M, Schulz PE. Disease-modifying effect of metabolic disorders in ALS/FTLD. Molecular Neurodegeneration. 2018;13:63.
Jawaid A, Woldemichael BT, Kremer EA, Gaur N, LaFerriere F, Polymenidou M, Mansuy IM. Memory decline and its reversal in aging and neurodegeneration involve miR-183/96/182 biogenesis. Molecular Neurobiology. 2018; 56:3451-62.
Paolicelli R, Jawaid A, Valeri A, Henstridge C, Merlini M, Robsinson JL, Lee EB, Appel S, Spires-Jones T, Lee VM, Trojanowski JQ, Schulz PE, Rajendran L. Increased microglial phagocytosis regulates enhanced amyloid clearance and synaptic pruning through TDP-43. Neuron. 2017;95:297-308.
Woldemichael BT*, Jawaid A*, Kremer EA, Gaur N, Krol J, Marchais A, Mansuy IM. The microRNAs cluster miR-183/96/182 contributes to long-term memory in a protein phosphatase 1-dependent manner. Nature Communications. 2016;7:12594.