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MCH/COX2-depend regulation of neuronal function and neuroinflammation in Alzheimer’s disease

Project description

Exploring the prodromal phase of Alzheimer’s disease

Alzheimer’s disease (AD) stays in a prodromal phase over many years before the manifestation of cognitive decline. Complex molecular and cellular alterations during the prodromal phase result in aberrant synaptic activity and chronic inflammation, leading to neuronal death. Preliminary data shows that melanin-concentrating hormone (MCH) synaptic regulatory function is impaired in a mouse model of early AD and AD patients. MCH regulates the expression of multiple genes that control neuronal activity and of cyclooxygenase-2 (COX2), which is essential for the synthesis of lipids involved in the inflammation process. The EU-funded SynLip project will study how MCH /COX2 interaction affects neuronal lipid metabolism and its contribution to neuroinflammation and the onset of cognitive decline.

Objective

Alzheimer’s disease (AD) patients stay in a prodromal phase over many years before robust cognitive decline. During this phase, complex molecular events lead to cellular alterations, resulting in aberrant synaptic activity and chronic inflammation which leads to neuronal death and cognitive impairment. My unpublished work, shows that melanin-concentrating hormone (MCH) regulates synaptic function and revealed that the MCH system is impaired in a mouse model of early AD and AD patients. I showed that MCH regulates the neuronal expression of multiple immediate early genes that control neuronal activity, and more interestingly the expression of Ptgs2/COX2. COX2 catalyzes the formation of pro-inflammatory prostaglandins from arachidonic acid but upon activity change it produces specialized pro-resolving mediators. Thus, precise COX2 levels and activity are essential to regulate the synthesis of bioactive lipids involved in the initiation and arrest of inflammation. Ptgs2/COX2 is expressed in excitatory neurons and a link to synaptic function, seizure and neuroinflammation-associated to seizure has been established. My preliminary data shows that excitatory neurons from a mouse model of early AD that displays MCH-system dysfunction, aberrant synaptic activity and neuroinflammation have altered Ptgs2 expression. Together with genetic studies that place lipid metabolism as a mediator of microglia-mediated neuroinflammation, this suggest that COX2 can play a critical role in the neuron-microglia interaction during the prodromal phase of AD. I hypothesize that impaired MCH system leads to aberrant neuronal activity and increased Ptgs2 expression, increasing pro-inflammatory mediators and recruiting microglia activation. Here, I will study how MCH-system/Ptgs2 interaction affects neuronal lipid metabolism and test if it regulates neuron-microglia communication contributing to neuroinflammation and to the onset of cognitive decline.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-WIDERA-2022-TALENTS-02

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Coordinator

UNIVERSIDADE DO MINHO
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 156 778,56
Address
LARGO DO PACO
4704 553 Braga
Portugal

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Region
Continente Norte Cávado
Activity type
Higher or Secondary Education Establishments
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Total cost

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