Acetylcholine, a neurotransmitter secreted by cholinergic neurons, is involved in signal transduction related to memory and learning ability. Alzheimer’s disease (AD), a progressive and commonly diagnosed neurodegenerative disease, is characterized by memory and cognitive decline and behavioral disorders. The pathogenesis of AD is complex and remains unclear, being affected by various factors. The cholinergic hypothesis is the earliest theory about the pathogenesis of AD. Cholinergic atrophy and cognitive decline are accelerated in age-related neurodegenerative diseases such as AD. In addition, abnormal central cholinergic changes can also induce abnormal phosphorylation of ttau protein, nerve cell inflammation, cell apoptosis, and other pathological phenomena, but the exact mechanism of action is still unclear. Due to the complex and unclear pathogenesis, effective methods to prevent and treat AD are unavailable, and research to explore novel therapeutic drugs is various and active in the world. This review summaries the role of cholinergic signaling and the correlation between the cholinergic signaling pathway with other risk factors in AD and provides the latest research about the efficient therapeutic drugs and treatment of AD.

The amyloid hypothesis of Alzheimer’s disease has long been the predominant theory, suggesting that Alzheimer’s disease is caused by the accumulation of amyloid beta protein (Aβ) in the brain, leading to neuronal toxicity in the central nervous system (CNS). Because of breakthroughs in molecular medicine, the amyloid pathway is thought to be central to the pathophysiology of Alzheimer’s disease (AD). Currently, it is believed that altered biochemistry of the Aβ cycle remains a central biological feature of AD and is a promising target for treatment. This review provides an overview of the process of amyloid formation, explaining the transition from amyloid precursor protein to amyloid beta protein. Moreover, we also reveal the relationship between autophagy, cerebral blood flow, ACHE, expression of LRP1, and amyloidosis. In addition, we discuss the detailed pathogenesis of amyloidosis, including oxidative damage, tau protein, NFTs, and neuronal damage. Finally, we list some ways to treat AD in terms of decreasing the accumulation of Aβ in the brain.

Cancer is one of the most prevalent diseases worldwide, and poses a threat to human health. Noncoding RNAs (ncRNAs) constitute most transcripts, but they cannot be translated into proteins. Studies have shown that ncRNAs can act as tumor suppressors or oncogenes. This review describes the role of several ncRNAs in various cancers, including microRNAs (miRNAs) such as the miR-34 family, let-7, miR-17-92 cluster, miR-210, and long noncoding RNAs (lncRNAs) such as HOX transcript antisense intergenic RNA (HOTAIR), Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), H19, NF-κB-interacting lncRNA (NKILA), as well as circular RNAs (circRNAs) and untranslated regions (UTRs), highlighting their effects on cancer growth, invasion, metastasis, angiogenesis, and apoptosis. They function as tumor suppressors or oncogenes that interfere with different axes and pathways, including p53 and IL-6, which are involved in the progression of cancer. The characteristic expression of some ncRNAs in cancer also allows them to be used as biomarkers for early diagnosis and therapeutic candidates. There is a complex network of interactions between ncRNAs, with some lncRNAs and circRNAs acting as competitive endogenous RNAs (ceRNAs) to decoy miRNAs and repress their expression. The ceRNA network is a part of the ncRNA network and numerous ncRNAs work as nodes or hubs in the network, and disruption of their interactions can cause cancer development. Therefore, the balance and stabilization of this network are important for cancer diagnosis and treatment.

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