https://www.selleckchem.com/products/iberdomide.html Low back pain (LBP) is prevalent and may transition into chronic LBP (cLBP) with associated reduced quality of life, pain, and disability. Because cLBP affects a heterogenous population, rehabilitation efforts must be individualized to meet the needs of various patient populations as well as individuals. This narrative review evaluated the many approaches to LBP rehabilitation including treatment-based classifications and specific types of rehabilitation efforts from exercise and physical therapy to spinal manipulation and bracing. Clinicians caring for patients with LBP or cLBP must be aware of the various options to find the right treatment course for each patient. In many cases, with proper patient expectations and care, nonpharmacological options may suffice to manage cLBP. While there is a rightful role for analgesics in the management of LBP, nonpharmacological options should be seriously considered, as they can play an important and health-sustaining role in patient management.Figure 1 caption was processed and published incorrectly. The correct caption should read as follows.Suppression of ubiquitin proteasome pathway (UPP) and stimulation of caspase-3 are involved in neurodegeneration. Can UPP activators and caspase-3 inhibitors ameliorate neurodegeneration? Here, we found a novel neuronal cell death accompanied with UPP activation and caspase-3 inhibition. Recently, plasmalemmal neuron-specific enolase (NSE) has been identified as one of membrane targets of 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2). 15d-PGJ2 induces neuronal apoptosis via activating caspase-3 and inactivating UPP, whereas the anti-NSE antibody inactivated caspase-3, activated UPP, and caused neuronal cell death. The anti-NSE antibody activated caspase-1 (pyroptosis marker), but not condense chromatin (apoptosis marker). The anti-NSE antibody declined intracellular level of ATP, which is not altered in pyroptosis. The intracellular leve