Limits...
Menopause, obesity and inflammation: interactive risk factors for Alzheimer's disease.

Christensen A, Pike CJ - Front Aging Neurosci (2015)

Bottom Line: Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder, the development of which is regulated by several environmental and genetic risk factors.The onset of menopause in mid-life elevates the vulnerability of women to AD, an increased risk that is likely associated with the depletion of estrogens.Menopause is also linked with an abundance of additional changes, including increased central adiposity and inflammation.

View Article: PubMed Central - PubMed

Affiliation: Davis School of Gerontology, University of Southern California Los Angeles, CA, USA.

ABSTRACT
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder, the development of which is regulated by several environmental and genetic risk factors. Two factors theorized to contribute to the initiation and/or progression of AD pathogenesis are age-related increases in inflammation and obesity. These factors may be particularly problematic in women. The onset of menopause in mid-life elevates the vulnerability of women to AD, an increased risk that is likely associated with the depletion of estrogens. Menopause is also linked with an abundance of additional changes, including increased central adiposity and inflammation. Here, we review the current literature to explore the interactions between obesity, inflammation, menopause and AD.

No MeSH data available.


Related in: MedlinePlus

Alzheimer’s disease (AD) is a multifactorial disorder in which multiple risk factors are theorized to interact in regulating pathogenesis. As depicted in the diagram an essential factor in AD is increasing age, which is also associated with elevated inflammation and, in women, menopause. The loss of estrogens at menopause increases central adiposity, which in turn increases inflammation and predisposes women to metabolic syndrome, insulin resistance, and AD. Individually and cooperatively, aging, menopause, adiposity, and inflammation lead to cognitive deficits and AD.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4493396&req=5

Figure 1: Alzheimer’s disease (AD) is a multifactorial disorder in which multiple risk factors are theorized to interact in regulating pathogenesis. As depicted in the diagram an essential factor in AD is increasing age, which is also associated with elevated inflammation and, in women, menopause. The loss of estrogens at menopause increases central adiposity, which in turn increases inflammation and predisposes women to metabolic syndrome, insulin resistance, and AD. Individually and cooperatively, aging, menopause, adiposity, and inflammation lead to cognitive deficits and AD.

Mentions: AD neuropathology is characterized and likely driven by the accumulation of Aβ and abnormally phosphorylated tau. The development of these and other components of AD neuropathology result from the interactive effects of several risk factors (Figure 1). Most importantly, AD is dependent upon aging. The negative outcomes of all genetic and environmental risk factors of AD require advancing age. In women, chronological aging is also tied to reproductive aging that is manifested as menopause in mid-life. Menopause results in cessation of the ovarian cycle and its cyclical production of estrogens and progesterone, sex steroid hormones with numerous protective roles against AD (Pike et al., 2009). Beyond protective actions against specific aspects of AD neuropathology, estrogens function throughout the body to guard against the development of increasing central adiposity and inflammation, both of which are implicated in the initiation and progression of AD. Of course, aging is also associated with significant increases in inflammation and central obesity, independent of estrogen levels. Thus, women are simultaneously exposed to the consequences of both chronological and reproductive aging, both of which can function as drivers of AD, obesity, and inflammation.


Menopause, obesity and inflammation: interactive risk factors for Alzheimer's disease.

Christensen A, Pike CJ - Front Aging Neurosci (2015)

Alzheimer’s disease (AD) is a multifactorial disorder in which multiple risk factors are theorized to interact in regulating pathogenesis. As depicted in the diagram an essential factor in AD is increasing age, which is also associated with elevated inflammation and, in women, menopause. The loss of estrogens at menopause increases central adiposity, which in turn increases inflammation and predisposes women to metabolic syndrome, insulin resistance, and AD. Individually and cooperatively, aging, menopause, adiposity, and inflammation lead to cognitive deficits and AD.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493396&req=5

Figure 1: Alzheimer’s disease (AD) is a multifactorial disorder in which multiple risk factors are theorized to interact in regulating pathogenesis. As depicted in the diagram an essential factor in AD is increasing age, which is also associated with elevated inflammation and, in women, menopause. The loss of estrogens at menopause increases central adiposity, which in turn increases inflammation and predisposes women to metabolic syndrome, insulin resistance, and AD. Individually and cooperatively, aging, menopause, adiposity, and inflammation lead to cognitive deficits and AD.
Mentions: AD neuropathology is characterized and likely driven by the accumulation of Aβ and abnormally phosphorylated tau. The development of these and other components of AD neuropathology result from the interactive effects of several risk factors (Figure 1). Most importantly, AD is dependent upon aging. The negative outcomes of all genetic and environmental risk factors of AD require advancing age. In women, chronological aging is also tied to reproductive aging that is manifested as menopause in mid-life. Menopause results in cessation of the ovarian cycle and its cyclical production of estrogens and progesterone, sex steroid hormones with numerous protective roles against AD (Pike et al., 2009). Beyond protective actions against specific aspects of AD neuropathology, estrogens function throughout the body to guard against the development of increasing central adiposity and inflammation, both of which are implicated in the initiation and progression of AD. Of course, aging is also associated with significant increases in inflammation and central obesity, independent of estrogen levels. Thus, women are simultaneously exposed to the consequences of both chronological and reproductive aging, both of which can function as drivers of AD, obesity, and inflammation.

Bottom Line: Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder, the development of which is regulated by several environmental and genetic risk factors.The onset of menopause in mid-life elevates the vulnerability of women to AD, an increased risk that is likely associated with the depletion of estrogens.Menopause is also linked with an abundance of additional changes, including increased central adiposity and inflammation.

View Article: PubMed Central - PubMed

Affiliation: Davis School of Gerontology, University of Southern California Los Angeles, CA, USA.

ABSTRACT
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder, the development of which is regulated by several environmental and genetic risk factors. Two factors theorized to contribute to the initiation and/or progression of AD pathogenesis are age-related increases in inflammation and obesity. These factors may be particularly problematic in women. The onset of menopause in mid-life elevates the vulnerability of women to AD, an increased risk that is likely associated with the depletion of estrogens. Menopause is also linked with an abundance of additional changes, including increased central adiposity and inflammation. Here, we review the current literature to explore the interactions between obesity, inflammation, menopause and AD.

No MeSH data available.


Related in: MedlinePlus