About this Research Topic
While the cause of Alzheimer’s Disease (AD) remains unknown, several risk factors have been linked to the pathogenesis of AD, including type 2 diabetes (T2DM). At the cellular and molecular level, both AD and T2DM share similar mechanistic abnormalities. Evidence has demonstrated that insulin resistance increases the risk of developing mild cognitive impairment, and AD. Changes in brain structure in insulin-resistant diabetes occur within temporal lobe circuits that are also sensitive to aging and AD, and individuals with insulin-resistant diabetes exhibit hippocampal atrophy. While these studies demonstrate a clear link between AD and T2DM the exact mechanisms through which T2DM contributes to cognitive decline in AD remains unexplored.
Considering insulin’s role in regulating brain homeostasis and function, it is not surprising that impaired insulin signaling has been linked with AD pathology. Findings show that insulin resistance and altered cerebral glucose utilization play an essential role in triggering AD-like pathology. Indeed, T2DM triggers an abnormal central inflammatory response, affecting hippocampal synaptic plasticity, learning, and memory. T2DM increases the expressions in the hippocampus of interleukin-1β (IL-1β), tumour necrosis factor α (TNF-α), and IL-6 in mice. Conversely, evidence shows that insulin administration enhances cognitive performance, and preserves volume changes in AD-related brain regions in patients . These observations demonstrate an intimate but unclear relationship between T2DM, and the cognitive deficits and neurodegeneration seen in AD patients.
This research topic focuses on investigating neuroinflammation and the central pathological effects of T2DM. Special focus will be on exploring the role of microglia and cytokines and their effect on synaptic function, neuronal health, and cognitive function in the diabetic state.
Specific themes that will be covered are:
1. Exploring mechanisms underlying neurodegeneration in T2DM.
2. Determining how aging impacts T2DM-induced neurodegeneration and cognition.
3. Determining the distinct T2DM-induced cognitive impairments and behaviors.
4. Exploring the role of microglia and cytokines in mediating T2DM-induced AD-like neuropathology.
5. Mechanisms underlying impairments in brain bioenergetics and glucose metabolism in T2DM and AD.
6. Therapeutic pathways to modulate neuroinflammation in the diabetic state.
Considering insulin’s role in regulating brain homeostasis and function, it is not surprising that impaired insulin signaling has been linked with AD pathology. Findings show that insulin resistance and altered cerebral glucose utilization play an essential role in triggering AD-like pathology. Indeed, T2DM triggers an abnormal central inflammatory response, affecting hippocampal synaptic plasticity, learning, and memory. T2DM increases the expressions in the hippocampus of interleukin-1β (IL-1β), tumour necrosis factor α (TNF-α), and IL-6 in mice. Conversely, evidence shows that insulin administration enhances cognitive performance, and preserves volume changes in AD-related brain regions in patients . These observations demonstrate an intimate but unclear relationship between T2DM, and the cognitive deficits and neurodegeneration seen in AD patients.
This research topic focuses on investigating neuroinflammation and the central pathological effects of T2DM. Special focus will be on exploring the role of microglia and cytokines and their effect on synaptic function, neuronal health, and cognitive function in the diabetic state.
Specific themes that will be covered are:
1. Exploring mechanisms underlying neurodegeneration in T2DM.
2. Determining how aging impacts T2DM-induced neurodegeneration and cognition.
3. Determining the distinct T2DM-induced cognitive impairments and behaviors.
4. Exploring the role of microglia and cytokines in mediating T2DM-induced AD-like neuropathology.
5. Mechanisms underlying impairments in brain bioenergetics and glucose metabolism in T2DM and AD.
6. Therapeutic pathways to modulate neuroinflammation in the diabetic state.
Keywords: Alzheimer’s Disease, Diabetes Mellitus, Neuroinflammation, Memory, Cytokines, Hippocampus, Aging
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