A Review and Hypothesized Model of the Mechanisms That Underpin the Relationship Between Inflammation and Cognition in the Elderly.

Masoumeh Tangestani Fard,Con Stough

doi:10.3389/fnagi.2019.00056

Masoumeh Tangestani Fard, Con Stough

Open Access

https://doi.org/10.3389/fnagi.2019.00056

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Abstract

Age is associated with increased risk for several disorders including dementias, cardiovascular disease, atherosclerosis, obesity, and diabetes. Age is also associated with cognitive decline particularly in cognitive domains associated with memory and processing speed. With increasing life expectancies in many countries, the number of people experiencing age-associated cognitive impairment is increasing and therefore from both economic and social terms the amelioration or slowing of cognitive aging is an important target for future research. However, the biological causes of age associated cognitive decline are not yet, well understood. In the current review, we outline the role of inflammation in cognitive aging and describe the role of several inflammatory processes, including inflamm-aging, vascular inflammation, and neuroinflammation which have both direct effect on brain function and indirect effects on brain function via changes in cardiovascular function.

Highlights

Life expectancies have increased considerably since the 1950s in developed countries
The findings showed that the concentration of tumor necrosis factor-α (TNF-α) and serum amyloid A, were higher in individuals with mild cognitive impairment (MCI) compared with cognitively normal participants (Trollor et al, 2010)
It is important to bear in mind that, there are normal or physiological levels of inflammation chronic events (Markiewski and Lambris, 2007; Fard et al, 2015; Sun et al, 2015; Tian et al, 2015; Arulselvan et al, 2016) may reshape a normal inflammatory response into an exaggerated response which could be characterized in terms of inflamm-aging, vascular inflammation and chronic neuroinflammation

Summary

INTRODUCTION

Life expectancies have increased considerably since the 1950s in developed countries. Several chronic vascular disorders are part of a progressive process, initiating and developing through local inflammation of large and medium sized arteries (Renna et al, 2013) It is scientifically relevant in this regard that pro-inflammatory signaling mechanism in the vascular wall has been well characterized and the risk of progressing age-associated neurodegenerative disease is related to increased circulatory inflammatory cytokines, such as IL-6 and TNFα (Simen et al, 2011). Most of the data available on vascular inflammation in relation to cognitive aging are based on animal models (Takeda et al, 2010; Yu et al, 2012; Won et al, 2013; Kaiser et al, 2014; Acharya et al, 2015) and available human studies mainly assess the role of systemic inflammatory biomarkers or symptomatic changes of cardiovascular risk factors in relation to cognitive aging. Future research should be conducted to include larger populations with longer observation, categorizing population via genetic, cognitive and behavioral phenotypes to study other factors, which could influence microglia activation (Figure 3)

DISCUSSION

Findings

LIMITATIONS AND FUTURE

CONCLUSION