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Review
. 2024 Aug 18;25(16):8982.
doi: 10.3390/ijms25168982.

Carotenoid Supplementation for Alleviating the Symptoms of Alzheimer's Disease

Affiliations
Review

Carotenoid Supplementation for Alleviating the Symptoms of Alzheimer's Disease

Jolanta Flieger et al. Int J Mol Sci. .

Abstract

Alzheimer's disease (AD) is characterized by, among other things, dementia and a decline in cognitive performance. In AD, dementia has neurodegenerative features and starts with mild cognitive impairment (MCI). Research indicates that apoptosis and neuronal loss occur in AD, in which oxidative stress plays an important role. Therefore, reducing oxidative stress with antioxidants is a natural strategy to prevent and slow down the progression of AD. Carotenoids are natural pigments commonly found in fruits and vegetables. They include lipophilic carotenes, such as lycopene, α- and β-carotenes, and more polar xanthophylls, for example, lutein, zeaxanthin, canthaxanthin, and β-cryptoxanthin. Carotenoids can cross the blood-brain barrier (BBB) and scavenge free radicals, especially singlet oxygen, which helps prevent the peroxidation of lipids abundant in the brain. As a result, carotenoids have neuroprotective potential. Numerous in vivo and in vitro studies, as well as randomized controlled trials, have mostly confirmed that carotenoids can help prevent neurodegeneration and alleviate cognitive impairment in AD. While carotenoids have not been officially approved as an AD therapy, they are indicated in the diet recommended for AD, including the consumption of products rich in carotenoids. This review summarizes the latest research findings supporting the potential use of carotenoids in preventing and alleviating AD symptoms. A literature review suggests that a diet rich in carotenoids should be promoted to avoid cognitive decline in AD. One of the goals of the food industry should be to encourage the enrichment of food products with functional substances, such as carotenoids, which may reduce the risk of neurodegenerative diseases.

Keywords: Alzheimer’s disease; brain; carotenoids; cognitive dysfunction; dementia; memory loss; natural products; neuroprotection.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Alzheimer’s disease KEGG pathway (hsa05010; Alzheimer disease—Homo sapiens (human)) generated online at https://www.genome.jp/kegg-bin/show_pathway?hsa05010, accessed on 8 March 2024) [115].
Figure 2
Figure 2
Chemical structure of lycopene–KEGG compound: C05432 [115].
Figure 3
Figure 3
The neuroprotective effect of lycopene in Alzheimer’s disease (AD) models. Abbreviations: mitochondrial permeability transition pore (mPTP), reactive oxidative species (ROS), mitochondria membrane potential (MMP), nuclear factor-κB (NF-κB), and amyloid precursor protein (APP)/amyloid precursor protein lyase 1 (BACE1). Malondialdehyde (MDA) decreases and glutathione peroxidase (GSH-Px) increases. Antiapoptotic Bcl-2 (the B-cell lymphoma-2) protein family is involved in the control of intracellular Ca2+ signaling. A high level of Bax/Bcl-2 is associated with greater vulnerability to apoptotic activation.
Figure 4
Figure 4
Chemical structures of α-carotene: KEGG Compound: C05433 (top), β-carotene-KEGG compound: C02094 (bottom) [115].
Figure 5
Figure 5
Chemical structures of lutein: KEGG compound: C08601 (top), and zeaxathin KEGG compound: C06098 (bottom) [115].
Figure 6
Figure 6
Chemical structures of astaxanthin–KEGG compound: C08580 [115].
Figure 7
Figure 7
Chemical structure of fucoxanthin–KEGG compound: C08596 [115].
Figure 8
Figure 8
Chemical structure of β-cryptoxanthin–KEGG compound: C08591 [115].
Figure 9
Figure 9
The cleavage pathways of β-cryptoxanthin.
Figure 10
Figure 10
Chemical structure of crocin–KEGG compound: C08589 [115].

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