Abstract

Aging and the emergence of age-associated illnesses are one of the major challenges of our present society. Alzheimer’s disease (AD) is closely associated with aging and is defined by increasing memory loss and severe dementia. Currently, there are no therapy options available that halt AD progression. This work investigates three hallmarks of the disease (autophagy, neuroinflammation, and senescence) and systematically analyzes if there is a beneficial effect from three substances derived from food sources, the so called “nutraceuticals” epigallocatechin gallate, fisetin, and spermidine, on these hallmarks. The results imply a positive outlook for the reviewed substances to qualify as a novel treatment option for AD. A combination of nutraceutical substances and other preventive measures could have significant clinical impact in a multi-layered therapy approach to counter AD.

Highlights

  • According to US Centers for Disease Control and Prevention (CDC) and the US National Institutes of Health (NIH), subjective cognitive decline (SCD) is the self-reported experience of worsening or more frequent confusion or memory loss

  • Cognitive decline can range from mild cognitive impairment to dementia, a form of decline in abilities severe enough to interfere with daily life

  • Epigallocatechin gallate (EGCG) is a polyphenol and flavonoid compound, both groups of chemicals that have been found to interfere with cascades that promote neuronal inflammation

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Summary

Introduction

According to US Centers for Disease Control and Prevention (CDC) and the US National Institutes of Health (NIH), subjective cognitive decline (SCD) is the self-reported experience of worsening or more frequent confusion or memory loss. It is a form of cognitive impairment and one of the earliest noticeable symptoms of Alzheimer’s disease (AD) and related dementias. Amyloid β (Aβ)-plaques and neurofibrillary tangles formed by tau protein aggregates have been discovered and linked to the disease. Because of their special role in the formation of AD, in this review the processes of autophagy, neuro-inflammation, and senescence are investigated

Autophagy and AD
Neuroinflammation and AD
Current Therapies and Limitations
EGCG and Autophagy
EGCG and Neuroinflammation
EGCG and Senescence
EGCG and AD
Fisetin
Fisetin and Autophagy
Fisetin and Neuroinflammation
Fisetin and Senescence
Fisetin and AD
Spermidine
Spermidine and Autophagy
Spermidine and Neuroinflammation
Spermidine and Senescence
Spermidine and AD
Findings
Discussion and Conclusions
Full Text
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