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How Do ApoE4 and Obesity Work Together to Drive Neuroinflammation and Alzheimer's Disease?
Late-onset Alzheimer’s disease (LOAD) accounts for 95% of all cases and is shaped by genetic and environmental factors. Emerging evidence shows that midlife obesity worsens cognitive deficits in ApoE4 carriers, pointing to a gene-environment interaction in LOAD pathogenesis. Our research explores how ApoE4 and obesity together intensify neuroinflammation by altering microglial plasticity and the brain’s immune landscape. |
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Uncovering the Link Between Vascular Dysfunction and Cognitive Impairment in Metabolic Disorders
Metabolic syndrome, including obesity and type 2 diabetes, affects 36.9% of U.S. adults and is a known risk factor for cognitive decline and Alzheimer’s disease. Systemic inflammation from these conditions contributes to vascular cognitive impairment and dementia (VCID), the second most common cause of dementia after Alzheimer's disease. However, the molecular mechanisms linking neuroinflammation, vascular dysfunction, and cognitive impairment remain unclear.
Our lab’s studies using a mouse model of obesity and type 2 diabetes revealed that obesity impairs cognitive and neurovascular function through inflammatory microglial activation, even in the absence of amyloid pathology.
Metabolic syndrome, including obesity and type 2 diabetes, affects 36.9% of U.S. adults and is a known risk factor for cognitive decline and Alzheimer’s disease. Systemic inflammation from these conditions contributes to vascular cognitive impairment and dementia (VCID), the second most common cause of dementia after Alzheimer's disease. However, the molecular mechanisms linking neuroinflammation, vascular dysfunction, and cognitive impairment remain unclear.
Our lab’s studies using a mouse model of obesity and type 2 diabetes revealed that obesity impairs cognitive and neurovascular function through inflammatory microglial activation, even in the absence of amyloid pathology.
Microglial Immune Memory and Its Implications for Alzheimer’s Disease
Persistent immune responses following viral infections, such as COVID-19, are increasingly linked to long-term neurological effects, yet their role in Alzheimer’s disease (AD) progression remains unclear. Our research investigates microglial immune memory—wherein microglia retain a "memory" of prior inflammatory events, potentially heightening neuroinflammation in AD. By elucidating the mechanisms underlying microglial priming, we aim to reveal how immune memory may contribute to AD pathology and inform novel strategies for modulating neuroinflammation in AD and related dementias.
Persistent immune responses following viral infections, such as COVID-19, are increasingly linked to long-term neurological effects, yet their role in Alzheimer’s disease (AD) progression remains unclear. Our research investigates microglial immune memory—wherein microglia retain a "memory" of prior inflammatory events, potentially heightening neuroinflammation in AD. By elucidating the mechanisms underlying microglial priming, we aim to reveal how immune memory may contribute to AD pathology and inform novel strategies for modulating neuroinflammation in AD and related dementias.