Title

Diet and nutrition, and their influence on Alzheimer’s disease and other neurodegenerative diseases

Document Type

Book Chapter

Publication Title

Neurodegeneration and Alzheimer's disease: The role of Diabetes, Genetics, Hormones, and Lifestyle

Publisher

Wiley

School

School of Medical and Health Sciences / Centre of Excellence for Alzheimer's Disease Research and Care

RAS ID

31528

Comments

Rainey‐Smith, S. R, Creegan, R., Fuller, S. J., Callisaya, M. L., Srikanth, V. (2019). Diet and nutrition, and their influence on Alzheimer's disease and other neurodegenerative diseases. In R. N. Martins, C. S. Brennan, W. M.A.D. B. Fernando, M. A. Brennan, S. J. Fuller (Eds.), Neurodegeneration and Alzheimer's disease: The role of diabetes, genetics, hormones, and lifestyle (pp. 117-147). Wiley. https://doi.org/10.1002/9781119356752.ch5

Abstract

Whilst the links between a healthy diet and healthy heart are firmly established and well documented, the relationship between diet and brain health is less well understood. Emerging research is ensuring however, that the maxim of ‘what is good for your heart, is also good for your brain’ is gaining momentum. Nutritional status and dietary habits have long been known to influence risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2D), and they are now materialising as key factors influencing Alzheimer's disease (AD) risk. This is compounded by the fact that both CVD and T2D are themselves risk factors for AD, and also by the fact that AD is an age‐related condition, and ageing is accompanied by an overall decline in digestive function, absorptive capabilities, and the assimilation of nutrients. Therefore, understanding the effect of macro‐ and micronutrients on neuronal biochemistry and AD pathology will provide opportunities for dietary manipulation to promote neuronal resistance to insults and reduce brain injury. This chapter discusses some of the key nutrients involved both directly in neuronal biochemistry, and indirectly by influencing peripheral metabolism, which in turn can modulate AD pathology.

DOI

10.1002/9781119356752.ch5

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