**5. Nervous system**

Bortezomib (C19H25BN4O4), or dipeptidyl boronic acid, is a proteasome inhibitor drug used in chemotherapy against hematologic malignancy. It has an anticancer activity. However, bortezomib often causes severe peripheral neuropathy. This condition has a special name such as "bortezomib-induced peripheral neuropathy (BIPN)." BIPN includes numbness and painful paraesthesia. Bortezomib has toxic effects on dorsal root ganglia via endoplasmic reticulum stress, protein carbonylation, and oxidative stress inducing. It also causes morphological changes in nervous system cells such as microglia [25, 26].

It was determined that infants exposed to 5–14 g boric acid or sodium tetraborate exerted such serious neuronal symptoms such as headache, tremor, convulsions, and even death after coma. These symptoms were associated with neuron degeneration, edema, and hemorrhage in the brain. However, chronical B deficiency causes such mental disorders as focusing problems, electroencephalogram changes, vigilance and psychomotor activity problems. B deficiency is strongly related to nervous system action potential problems [27]. In another study, Ozansoy et al. demonstrated that sodium borate decahydrate and boric acid administrations improved amyloid-beta

toxicity in SH-SY5Y cells in vitro via increased expression levels of Sirt1 and regulated GSK-3α/β expressions [28].

Thus, this information suggested that B and B compounds could have U-shaped effects in the nervous system. Excessive B and B compounds exposure causes toxicity, and deficiency causes neuron metabolic pathway problems, and even B and B compounds could be possible therapy options for neurological diseases.
