Research
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Our long-term goal is to determine how sex, aging, and sex hormones influence vascular and metabolic contributions to dementia and to develop sex-specific therapeutic strategies to improve cognitive function and reduce the burden of dementia.
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Current Projects:
1) Sex differences in effects of prediabetes on vascular contributions to cognitive impairment and dementia (VCID).
VCID is the second leading cause of dementia. Diabetes impairs vascular function and is a major risk factor for VCID. Vascular effects of diabetes are greater in females than males, however, little is known regarding the effects of prediabetes. We have found that prediabetes causes more severe cognitive impairment in females compared to males using a mouse model of VCID. Currently we are determining sex differences in the underlying neuro-, glial-, and vascular pathology. This project was funded by an American Heart Association Scientist Development Grant.
2) Metabolic & hormonal mechanisms of VCID.
Risk of VCID is significantly increased in metabolically impaired (prediabetic/diabetic) post-menopausal women. This study will determine if menopause exacerbates the effects of prediabetes on VCID pathology and cognitive deficits. Further, will determine if these effects can be reversed by increasing estrogen specifically in the brain. Our study will provide mechanistic insight that will facilitate future interventions to decrease the burden of dementia, particularly in the high-risk population of prediabetic post-menopausal women. This project is funded by an R01 from NINDS.
3) Sex differences in vascular contributions to Alzheimer's disease.
Up to 80% of those with Alzheimer's disease have underlying vascular damage (VCID) and/or metabolic disease (prediabetes or diabetes). Alzheimer's disease is more prevalent in women than men. The goal of this study is to determine sex differences in how metabolic disease and VCID alter Alzheimer's disease pathology and cognitive deficits using mouse models. This project was funded by Albany Medical College Start Up funds.
4) Influence of menopause and metabolic disease on Alzheimer's disease.
Approximately 2/3 of those with Alzheimer’s disease (AD) are women, the majority of which are post-menopausal. Menopause accelerates mid-life risk factors for AD, by increasing risk for both vascular and metabolic diseases. The objective of this proposal is to understand the important interaction between menopause and metabolic disease on AD pathology. We hypothesize that cognitive deficits and neuropathology induced by obesity/prediabetes will be worse in post-menopausal AD females and will be reversed by increasing estradiol specifically in the brain. This project is funded by the Alzheimer's Association.
5) Neuroimmune changes with aging and dementia.
Neuroinflammation is known to increase with both aging and dementia. In collaboration with Dr. Qi Yang's lab, we are assessing changes in a novel type of anti-inflammatory immune cell in the brain - group type 2 innate lymphoid cells (ILC2s). Activating these cells is showing promise in protecting against age-related decline in our mouse models. To hear more about this work, check out our recent interview in Newsweek.
6) Investigating the functional impact of Alzheimer's disease fisk genes in neuro-vascular interactions.
Vascular pathology is found in up to 80% of all Alzheimer's disease cases. In a multi-PI collaboration (with Dr. Sally Temple, Dr. Celeste Karch, Dr. Oscar Harari, Dr. Martin Kampmann, and Dr. Kevin Pumiglia), we are identifying key vascular risk genes for Alzheimer's disease and characterizing their impact on both vascular and cognitive function in several mouse models of Alzheimer's disease. This work is funded by National Institute on Aging as a U01 consortium grant.
1) Sex differences in effects of prediabetes on vascular contributions to cognitive impairment and dementia (VCID).
VCID is the second leading cause of dementia. Diabetes impairs vascular function and is a major risk factor for VCID. Vascular effects of diabetes are greater in females than males, however, little is known regarding the effects of prediabetes. We have found that prediabetes causes more severe cognitive impairment in females compared to males using a mouse model of VCID. Currently we are determining sex differences in the underlying neuro-, glial-, and vascular pathology. This project was funded by an American Heart Association Scientist Development Grant.
2) Metabolic & hormonal mechanisms of VCID.
Risk of VCID is significantly increased in metabolically impaired (prediabetic/diabetic) post-menopausal women. This study will determine if menopause exacerbates the effects of prediabetes on VCID pathology and cognitive deficits. Further, will determine if these effects can be reversed by increasing estrogen specifically in the brain. Our study will provide mechanistic insight that will facilitate future interventions to decrease the burden of dementia, particularly in the high-risk population of prediabetic post-menopausal women. This project is funded by an R01 from NINDS.
3) Sex differences in vascular contributions to Alzheimer's disease.
Up to 80% of those with Alzheimer's disease have underlying vascular damage (VCID) and/or metabolic disease (prediabetes or diabetes). Alzheimer's disease is more prevalent in women than men. The goal of this study is to determine sex differences in how metabolic disease and VCID alter Alzheimer's disease pathology and cognitive deficits using mouse models. This project was funded by Albany Medical College Start Up funds.
4) Influence of menopause and metabolic disease on Alzheimer's disease.
Approximately 2/3 of those with Alzheimer’s disease (AD) are women, the majority of which are post-menopausal. Menopause accelerates mid-life risk factors for AD, by increasing risk for both vascular and metabolic diseases. The objective of this proposal is to understand the important interaction between menopause and metabolic disease on AD pathology. We hypothesize that cognitive deficits and neuropathology induced by obesity/prediabetes will be worse in post-menopausal AD females and will be reversed by increasing estradiol specifically in the brain. This project is funded by the Alzheimer's Association.
5) Neuroimmune changes with aging and dementia.
Neuroinflammation is known to increase with both aging and dementia. In collaboration with Dr. Qi Yang's lab, we are assessing changes in a novel type of anti-inflammatory immune cell in the brain - group type 2 innate lymphoid cells (ILC2s). Activating these cells is showing promise in protecting against age-related decline in our mouse models. To hear more about this work, check out our recent interview in Newsweek.
6) Investigating the functional impact of Alzheimer's disease fisk genes in neuro-vascular interactions.
Vascular pathology is found in up to 80% of all Alzheimer's disease cases. In a multi-PI collaboration (with Dr. Sally Temple, Dr. Celeste Karch, Dr. Oscar Harari, Dr. Martin Kampmann, and Dr. Kevin Pumiglia), we are identifying key vascular risk genes for Alzheimer's disease and characterizing their impact on both vascular and cognitive function in several mouse models of Alzheimer's disease. This work is funded by National Institute on Aging as a U01 consortium grant.
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