Alzheimer’s disease (AD) is the most common type of dementia, increasing by 10 new cases every day in Saskatchewan alone. AD results from pathological amyloid beta (Aβ) peptides that hamper neurons’ communication, cause progressive neuronal cell death in the central nervous system, and ultimately lead to memory loss in the individual. While disease symptoms are well known, the mechanism by which Aβ triggers the degeneration of the brain remains elusive. There is no cure for AD and present treatments only focus on slowing down the disease progression or mitigating symptoms. This study has used several techniques to investigate the effect of Aβ on the electrophysiology and morphology of isolated hippocampal and dorsal root ganglion (DRG) neurons in order to test whether the effects of Aβ exposure and clearance are exclusive to central nervous system neurons. Isolation and culture of hippocampal and DRG neurons were performed. By exposing neurons to combinations of Aβ42 and Aβ38, electrophysiological and morphological techniques were used to assess the effects of Aβ on neuronal cells. Using patch clamp electrophysiology, I demonstrated a significant decrease in the current density profile of neurons after 24-h of exposure to Aβ42 and Aβ38. Additionally, Aβ had a dose-dependent effect on hippocampal and DRG neurons’ morphology, reducing neuronal soma and nucleus size. The addition of Aβ38 negated the depressive effect of Aβ42, suggesting the cancellation of low current density profiles of neurons or the inhibition of their electrical activity. Thus, co-treatment of Aβ42 and Aβ38 neutralized the depressive Aβ effect on neuronal cells. This research has demonstrated the electrophysiology of hippocampal and DRG neurons after Aβ exposure to understand the fundamental biology of Aβ exposure at a cellular level, which is involved in the pathophysiology of AD and other types of dementia.