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Review
. 2023 Mar 8;13(3):457.
doi: 10.3390/brainsci13030457.

Carotenoids: Role in Neurodegenerative Diseases Remediation

Kumaraswamy Gandla  1 , Ancha Kishore Babu  2 , Aziz Unnisa  3 , Indu Sharma  4 , Laliteshwar Pratap Singh  5 , Mahammad Akiful Haque  6 , Neelam Laxman Dashputre  7 , Shahajan Baig  8 , Falak A Siddiqui  9 , Mayeen Uddin Khandaker  10 , Abdullah Almujally  11 , Nissren Tamam  12 , Abdelmoneim Sulieman  13 , Sharuk L Khan  9 , Talha Bin Emran  14   15
Affiliations
Review

Carotenoids: Role in Neurodegenerative Diseases Remediation

Kumaraswamy Gandla et al. Brain Sci. .

Abstract

Numerous factors can contribute to the development of neurodegenerative disorders (NDs), such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Oxidative stress (OS), a fairly common ND symptom, can be caused by more reactive oxygen species being made. In addition, the pathological state of NDs, which includes a high number of protein aggregates, could make chronic inflammation worse by activating microglia. Carotenoids, often known as "CTs", are pigments that exist naturally and play a vital role in the prevention of several brain illnesses. CTs are organic pigments with major significance in ND prevention. More than 600 CTs have been discovered in nature, and they may be found in a wide variety of creatures. Different forms of CTs are responsible for the red, yellow, and orange pigments seen in many animals and plants. Because of their unique structure, CTs exhibit a wide range of bioactive effects, such as anti-inflammatory and antioxidant effects. The preventive effects of CTs have led researchers to find a strong correlation between CT levels in the body and the avoidance and treatment of several ailments, including NDs. To further understand the connection between OS, neuroinflammation, and NDs, a literature review has been compiled. In addition, we have focused on the anti-inflammatory and antioxidant properties of CTs for the treatment and management of NDs.

Keywords: carotenoids; neurodegeneration; neuroinflammation; oxidative stress; reactive oxygen species.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Endogeneous sources of ROS and RNS. Where, ROS, reactive oxygen species; RNS, reactive nitrogen species; CYP, cytochrome; NOS, nitric oxide synthase.
Figure 2
Figure 2
The oxidative process that is required to convert inactive retinol into useful retinoic acid takes place in two stages. Where, ADH, alcohol dehydrogenases; RALDH, retinaldehyde dehydrogenase.
Figure 3
Figure 3
The constituent molecules that make up the chemical structure of various common plasma carotenoids.
Figure 4
Figure 4
Carotenoids and the signaling pathways involved in inflammation. MAPK, mitogen-activated protein kinase; ROS, reactive oxygen species; Nrf2, nuclear factor erythroid 2–related factor 2; SOD, superoxide dismutase, RAS, rat sarcoma.
Figure 5
Figure 5
The mechanism by which Nrf2 promotes expression of genes that contain the ARE element. The migration of Nrf2 to the nucleus is made possible by the disruption of the Keap1–Nrf2 complex [47].
Figure 6
Figure 6
Carotenoids’ protective functions during neuronal death. Reactive oxygen species (ROS) can initiate apoptosis via the death receptor pathway and the mitochondrial route. (Reactive oxygen species (ROS); mitogen-activated and extracellular-signal-regulated kinase kinases (MEK); extracellular-signal-regulated kinases (ERK); nuclear factor (erythroid-derived 2)-such as 2 (Nrf2); impaired antioxidant (Keap1); small Maf proteins (sMaf); antioxidant response element (ARE); phosphoinositide 3-kinase (PI3K); protein kinase B (Akt); nuclear factor-κB (NF-κB); membrane-targeted death ligand (tBid); apoptosis regulator (BAX); B-cell lymphoma (Bcl-xl)).
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