Cancer is a major public health problem, and chemotherapy plays a significant role in the management of neoplastic diseases. However, chemotherapy-induced cardiotoxicity is a serious side effect secondary to cardiac damage caused by antineoplastic's direct and indirect toxicity. Currently, there are no reliable and approved methods for preventing or treating chemotherapy-induced cardiotoxicity. Understanding the mechanisms of chemotherapy-induced cardiotoxicity may be vital to improving survival. The independent risk factors for developing cardiotoxicity must be considered to prevent myocardial damage without decreasing the therapeutic efficacy of cancer treatment. This systematic review aimed to identify and analyze the evidence on chemotherapy-induced cardiotoxicity, associated risk factors, and methods to decrease or prevent it. We conducted a comprehensive search on PubMed, Google Scholar, and Directory of Open Access Journals (DOAJ) using the following keywords: "doxorubicin cardiotoxicity", "anthracycline cardiotoxicity", "chemotherapy", "digoxin decrease cardiotoxicity", "ATG7 activators", retrieving 59 articles fulfilling the inclusion criteria. Therapeutic schemes can be changed by choosing prolonged infusion application over boluses. In addition, some agents like Dexrazoxane can reduce chemotherapy-induced cardiotoxicity in high-risk groups. Recent research found that Digoxin, ATG7 activators, Resveratrol, and other medical substances or herbal compounds have a comparable effect on Dexrazoxane in anthracycline-induced cardiotoxicity.

Alzheimer’s disease (AD) is a neurological disorder characterized by mental and behavioral changes that develop progressively with a decline in brain function. Dysfunctions in glutamatergic and cholinergic pathways, along with an increased concentration of beta-amyloid protein (Aβ), lead to synapses that are full of phosphorylated protein. These changes result in several pathological, biochemical, cellular, and molecular alterations that increase neural excitation directly or indirectly at the neural level, affecting the synapse, axons, signal transmission, and all parts of neurons. All these alterations, with continuous excitatory effects, eventually lead to neural loss and degradation due to stimulation of the immune response. However, memantine is a non-competitive antagonist of N-methyl-D-aspartic acid (NMDA) glutamatergic receptors of moderate affinity and voltage-dependent that blocks the effects of pathologically elevated glutamate tonic levels, which can lead to neuronal dysfunction. Memantine has shown improvement in cognition, global clinical status, activities of daily living, and behavioral disturbances in moderate and severe AD. In this review, we will discuss the effects of memantine use and side effects, as well as its application in treating other diseases or pathological conditions with the prospective use of memantine or an alternative. Memantine is generally well-tolerated, and the most common adverse reactions are vertigo, headache, and hallucinations, which are usually mild.