In the process of neuronal inflammation, an increased in inflammatory cytokines (IL-1β, IL-6 and TNF-α) from immune cells (leukocytes and macrophages), brain cells (microglia, astrocytes and neurons) and in hippocampus, amygdala occurs. Raise the level of cytokines result in reduced in production of molecules that are related to plasticity, especially BDNF, IGF-1 and VEGF. Microglia activation lead to suppression of neurogenesis, differentiation of NPCs, decrease in long-term potentiation (LTP) and induction of learning and memory impairment. Also, the phenomenon of nerve inflammation with an increase in the level of TNFα cause inhibition of astrocytes in the removal of glutamate and led to neuronal death. Elevated in TNFα level result in increased activity of the iNOS enzyme that is available in astrocytes in the CA1 hippocampus and it is responsible for increase in oxidant molecules and depression of LTP. Furthermore, the increase in inflammatory reaction mediators result in subsequent neurotoxic consequences. Indeed, inflammatory factors deliberate as a predisposing agent for neurodegenerative disease. Boswellia serrate from Burseracea family, it's resin (Frankincense or Ollibanum) and the main constituent of this resin (boswellic acid) play important role in suppression of neuronal inflammation with inhibition of 5-lipoxygenase, Prostaglandin E2 formation and expression of inflammatory cytokines and chemokines. Boswellia serrate and its derivatives with anti-inflammatory properties have therapeutic effects on memory retention, decrease in brain edema, facilitation in nerve impulse, improve the pathogenesis of neuroinflammatory disease like Alzheimer's disease.

Many chemicals with broad industrial, pharmaceutical and agricultural application produce a neurotoxic syndrome in humans and experimental animals involving weight loss, skeletal muscle weakness and ataxia. Neurotoxicity is defined as a structural change or a functional alteration of the nervous system resulting from exposure to a chemical, biological or physical agent. Neurotoxicity including Neuronopathia, Axonopathia and myelopathies. The causes of Neuropathies Are Doxorubicin, Methyl Mercury. Axonopathies causes of Gamma-Diketones, β′-Iminodipropionitrile, Acrylamide and Myelopathies causes of Hexachlorophene Tellurium, Lead. Acrylamide (ACR) as a chemical industry is a poison in foods prepared at high temperatures and is the most important neurotoxic agent. Humans that workers in factories are more susceptible for peripheral neuropathies of these toxic agent at high doses. The first symptoms are observed in Pacinian corpuscles, muscle spindles and the nerve terminal. These side effects is result from additions of neurofilaments at the nerve terminal. Developing of Para nodal swellings, cause myelin withdrawal. In additional, Acrylamide lead to sensory axonopathy, Axonal degeneration and peripheral neuropathy. In study mention that, mild ataxia, typical ataxia and hind limb weakness were appeared with 10 mg/kg and 20 mg/kg respectively. The GAP-43 protein marker, is tested for assess of neuronal function that is related to hippocampal neuronal growth, promoting axonal elongation and retaining axonal morphology. Also GAP-43 protein may modulate the transmission of neural signals because of extensively distribution at the axonal terminate. ACR exposure cause inhibition of expression of GAP-43, so may result in disturbance in axonal growth, synaptic terminal vesicles, mitochondria, synaptic inhibition and eventually, terminate the retrograde and anterograde axonal transport. In more recent studies were suggested that ACR, even in its low-dose, can lead to neurological symptoms and nerve terminal degeneration like axonopathy.