Conjecturable role of aluminum in pathophysiology of stroke

Abstract

Escalated environmental contamination and extensive use of aluminum in the contemporary life made its exposure inevitable. Increased uses of aluminum nanoparticles in health applications are widening its impacts. Targeted accumulation of aluminum in nonrenewable cells of brain has nullified the benefits of restricted bioavailability and assimilation, and lead to the contended involvement of the metal in neurodegenerative disorders. In addition to this, special features of aluminum have coerced to evaluate its influence on the pathophysiology of stroke. The wallops of aluminum on aging, cerebrovascular dysfunction, atherogenesis, blood-brain barrier, matrix metalloproteinases, platelet reaction, and homocysteine are discussed to divulge the ways which can aggravate risk factors of stroke. Region-specific susceptibility of aluminum assails and ischemic stroke are compared to predict the link between these neurodegenerative causations. Sequence of pathophysiological changes in stroke are discussed in terms of energy inadequacy, ion-pump failure, depolarization, alteration in [Ca2+]ICF, mitochondrial dysfunction, excitotoxicity, generation of free radicals and inflammatory mediators, and mechanism of cell death are evaluated with aluminum-mediated similar changes and possible influence of aluminum has been indicated in the stroke pathophysiology. In the same line, positive and negative possibilities of aluminum are also speculated in poststroke neuroresuscitation and postconditioning neuroprotection.