Alexei Verkhratsky, (Ukrainian: Олексій Верхратський,[2] Russian: Алексей Верхратский[3]) sometimes spelled Alexej, is a professor of neurophysiology at the University of Manchester best known for his research on the physiology and pathophysiology of neuroglia, calcium signalling, and brain ageing.

His father is Nestor Verkhratsky (Верхратський Нестoр Сергійович), a gerontologist who headed a laboratory at the Institute of Gerontology of the National Academy of Sciences of Ukraine.

Moving to the UK in 1999, he has held multiple positions at the University of Manchester including senior lecturer, reader, professor and chairman in the School of Biological Sciences.

In 1990, Verkhratsky discovered functional expression of low- and high-threshold Ca2+ channels in oligodendroglial precursors, this is the earliest finding underlying the concept of electrical excitability of NG2-glia.

Subsequently, he identified a unique expression of highly ATP-sensitive P2X1/5 receptors in cortical astrocytes and characterised their role in translating neuronal synaptic activity to astroglial [Ca2+]i signalling.

[17] The development of this concept begun from the very first recordings of astroglial Na+ signals in response to physiological stimulation in situ in cerebellar Bergmann radial astrocytes.

In a series of highly cited conceptual reviews he outlined basic principles of glial physiology and pathophysiology, which significantly influenced this rapidly developing area of neuroscience.

First, in collaboration with Rodriguez, he discovered prominent inhibition of neurogenesis (linked to the radial astrocytes-neural stem cells) in the animal model of Alzheimer's disease.

[26] Subsequently, he discovered morphological and functional evidence for astroglial atrophy at the early stages of AD that preceded the appearance of the typical neuronal histopathology in animal models;[27] these observations have been subsequently corroborated in experiments on astrocytes differentiated from pluripotent stem cells obtained from patients with clinically confirmed Alzheimer's disease in both familial and sporadic forms.