Neuroprotective and Anti-Aging Potentials of Essential Oils from Aromatic and Medicinal Plants

Abstract

The use of essential oils (EOs) and their components is known since long in traditional medicine and aromatherapy for the management of various diseases, and is further increased in the recent times. The neuroprotective and anti-aging potentials of EOs and their possible mechanism of actions were evaluated by numerous researchers around the globe. Several clinically important EOs and their components from Nigella sativa, Acorus gramineus, Lavandula angustifolia, Eucalyptus globulus, Mentha piperita, Rosmarinus officinalis, Jasminum sambac, Piper nigrum and so many other plants are reported for neuroprotective effects. This review article was aimed to summarize the current finding on EOs tested against neurodegenerative disorders like Alzheimer disease (AD) and dementia. The effects of EOs on pathological targets of AD and dementia including amyloid deposition (Aβ), neurofibrillary tangles (NFTs), cholinergic hypofunction, oxidative stress and glutamatergic abnormalities were focused. Furthermore, effects of EOs on other neurological disorders including anxiety, depression, cognitive hypofunction epilepsy and convulsions were also evaluated in detail. In conclusion, EOs were effective on several pathological targets and have improved cognitive performance in animal models and human subjects. Thus, EOs can be developed as multi-potent agents against neurological disorders with better efficacy, safety and cost effectiveness.

Keywords: Alzheimer’s disease; BACE1; NFTs; amyloid-β; antioxidants; cholinesterase inhibitors; dementia; essential oils.

Figure 1

Chemical structures of most abundant and therapeutically active compounds in essential oils (EOs).

Figure 2

Clinically available anti-Alzheimer drugs. Donepezil, Galanthamine, Rivastigmine and Tacrine are cholinesterase inhibitors whereas, Memantine is N-methyl-d-aspartate (NMDA) receptor antagonist.

Figure 3

Neuronal synthesis of acetylcholine (ACh). ACh is stored in the vesicles and subsequent to action potential they get fused with the membrane and release the ACh at neuronal junction. After their action on cholinergic receptors they are enzymatically cleaved by acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). EOs can inhibit the action of these cholinesterase’s and can restore their action for prolong time. Thus they are useful for the symptomatic management of Alzheimer disease (AD).

Figure 4

Schematic presentation of amyloidogenic pathway and formation of amyloid-β (Aβ) in AD. The amyloidogenic process is initiated by the enzymatic breakdown of amyloid precursor protein (APP) by beta amyloid cleaving enzyme (BACE1) called beta secretase at beta site. This is followed by catalytic cleavage of APP by gamma secretase to form non-soluble protein or Aβ. This Aβ accumulation in the neurons leading to impairment in the neurotransmission and neurodegeneration. EOs can inhibit the activity of BACE1 to hamper the Aβ load.

Figure 5

The figure summarize various sources of free radicals production with special focus on Aβ as initiator of reactive oxygen species (ROS) and reactive nitrogen species (RNS). After generation, the free radicals attack membrane lipids, cellular organelles which leads to the production of mitochondrial toxins hydroxynonenal (HNE) and malondialdehyde. Oxidative stress damage membrane-bound ion-selective ATPases and stimulate calcium influx via stimulation of NMDA receptors, membrane attack complex (MAC), and ion-specific Aβ pore formation with ultimate increase in cytosolic and mitochondrial calcium load. Cellular amyloid targets cytochrome c oxidase, α-ketoglutarate and pyruvate dehydrogenase and thus cause mitochondrial DNA damage causing its fragmentation. Lipid peroxidation products enhance phosphorylation and aggregation of tau proteins which subsequently inhibit complex I. Excessive quantities of ROS and RNS are produced at complexes I and III. Further, the mitochondrial membrane potential (MMP) crumple and permeability-transition pores (ψm) opened leading to activation of caspases. Aβ also stimulate the production of stress-induced protein kinases (p38) and c-jun N-terminal kinase (JNK), in addition to p53, which stimulate apoptosis leading to cellular damage.

Figure 6

Summary of the pathological targets in AD.