Item Details

title

CHARACTERIZING ALZHEIMER’S DISEASE PATHOLOGY AND MOLECULAR SIGNALING DYSREGULATION IN AGED CYNOMOLGUS MACAQUES WITH NORMAL AND HIGH BLOOD GLUCOSE

author

Jester, Hannah Marie

abstract

Alzheimer’s disease (AD) is one of the most prevalent health concerns in our society today. There are 5.8 million people currently diagnosed with AD in the United States alone, and this number is only expected to increase as more of the population gets older. The underlying mechanisms of AD are still unknown and this has largely prevented the development of efficacious therapies or treatments. There are numerous factors that contribute to a person’s risk of developing AD. In terms of modifiable risk factors, many are metabolic in nature and contribute to risk of cardiovascular disease as well. These include type 2 diabetes mellitus (T2DM), obesity, insulin resistance, and elevated glucose levels. It has been determined that those with T2DM have a 73% higher relative risk for developing any type of dementia than those without T2DM, and a 56% increased risk for developing Alzheimer’s disease specifically. Several studies have associated insulin resistance and T2DM with cognitive decline. The increased risk and comorbidity of these metabolic disorders with AD have led to questions about possible common etiologies or underlying mechanisms of these diseases. Indeed, there are pathophysiological elements common among metabolic disorders and AD that are detrimental to synaptic plasticity and cognitive function. Non-human primate (NHP) models of T2DM and AD may prove to be incredibly useful in understanding the molecular links between T2DM and AD since both diseases are naturally occurring in many species of NHPs.

subject

Alzheimer's

Diabetes

Insulin Resistance

Molecular signaling

Non-human primates

Pathology

contributor

Ma, Tao (committee chair)

Macauley-Rambach, Shannon L (committee member)

Ko, Mei-Chuan (committee member)

date

2020-05-29T08:36:04Z (accessioned)

2020-05-29T08:36:04Z (available)

2020 (issued)

degree

Neuroscience – MS (discipline)

identifier

http://hdl.handle.net/10339/96830 (uri)

language

en (iso)

publisher

Wake Forest University

type

Thesis