Aging, Cellular Senescence, and Alzheimer’s Disease

Liu, Rui-Ming

doi:10.3390/ijms23041989

Cited by 80 publications

(21 citation statements)

References 112 publications

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“…Cellular senescence, a state of permanent cell growth arrest, is believed to contribute importantly to aging and aging-related diseases (e.g., AD, cancer, pulmonary fibrosis). In addition, senescent astrocytes, microglia, endothelial cells, and neurons have been detected in the brain of AD patients and AD animal models ( Liu, 2022 ). Nonetheless, although accumulated evidence highlights the role of cellular senescence in aging and AD, the mechanisms that promote cell senescence and how senescent cells contribute to AD neuro-pathophysiology remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of Aging-Related Genes in Alzheimer’s Disease

Zhang

Weng

2022

Front. Neurosci.

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Aging is recognized as the key risk factor for Alzheimer’s disease (AD). This study aimed to identify and verify potential aging-related genes associated with AD using bioinformatics analysis. Aging-related differential expression genes (ARDEGs) were determined by the intersection of limma test, weighted correlation network analysis (WGCNA), and 1153 aging and senescence-associated genes. Potential biological functions and pathways of ARDEGs were determined by GO, KEGG, GSEA, and GSVA. Then, LASSO algorithm was used to identify the hub genes and the diagnostic ability of the five ARDEGs in discriminating AD from the healthy control samples. Further, the correlation between hub ARDEGs and clinical characteristics was explored. Finally, the expression level of the five ARDEGs was validated using other four GEO datasets and blood samples of patients with AD and healthy individuals. Five ARDEGs (GFAP, PDGFRB, PLOD1, MAP4K4, and NFKBIA) were obtained. For biological function analysis, aging, cellular senescence, and Ras protein signal transduction regulation were enriched. Diagnostic ability of the five ARDEGs in discriminating AD from the control samples demonstrated a favorable diagnostic value. Eventually, quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) validation test revealed that compared with healthy controls, the mRNA expression level of PDGFRB, PLOD1, MAP4K4, and NFKBIA were elevated in AD patients. In conclusion, this study identified four ARDEGs (PDGFRB, PLOD1, MAP4K4, and NFKBIA) associated with AD. They provide an insight into potential novel biomarkers for diagnosing AD and monitoring progression.

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Section: Discussionmentioning

confidence: 99%

Identification and Validation of Aging-Related Genes in Alzheimer’s Disease

Zhang

Weng

2022

Front. Neurosci.

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“…In addition to possible genetic factors, a variety of acquired factors can lead to the development of AD. Aging or cellular senescence is believed to contribute importantly to aging and aging-related diseases, including LOAD ( Liu, 2022 ). Early life stress and environmental neurotoxic may be risk factors for the initiation and progression of LOAD ( Gauvrit et al, 2022 ; Tsamou et al, 2022 ).…”

Section: Etiology Of Alzheimer’s Diseasementioning

confidence: 99%

Cellular Reprogramming and Its Potential Application in Alzheimer’s Disease

Zhou

Zhu

et al. 2022

Front. Neurosci.

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Alzheimer’s disease (AD) has become the most common age-related dementia in the world and is currently incurable. Although many efforts have been made, the underlying mechanisms of AD remain unclear. Extracellular amyloid-beta deposition, intracellular tau hyperphosphorylation, neuronal death, glial cell activation, white matter damage, blood–brain barrier disruption, and other mechanisms all take part in this complicated disease, making it difficult to find an effective therapy. In the study of therapeutic methods, how to restore functional neurons and integrate myelin becomes the main point. In recent years, with the improvement and maturity of induced pluripotent stem cell technology and direct cell reprogramming technology, it has become possible to induce non-neuronal cells, such as fibroblasts or glial cells, directly into neuronal cells in vitro and in vivo. Remarkably, the induced neurons are functional and capable of entering the local neural net. These encouraging results provide a potential new approach for AD therapy. In this review, we summarized the characteristics of AD, the reprogramming technique, and the current research on the application of cellular reprogramming in AD. The existing problems regarding cellular reprogramming and its therapeutic potential for AD were also reviewed.

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“…Alzheimer’s disease is the leading cause of dementia worldwide, inducing progressive impairment of cognitive function that seriously affects daily life ( Liu, 2022 ). After age 65 years, the incidence of AD approximately doubles every 5 years, and 50% of the population aged ≥ 85 years has AD ( Winblad et al, 2016 ).…”

Section: Hotair Involvement In Pathogenesis Of Central Nervous System...mentioning

confidence: 99%

Long Non-coding RNA HOTAIR in Central Nervous System Disorders: New Insights in Pathogenesis, Diagnosis, and Therapeutic Potential

Wang

Zhao

Pan

et al. 2022

Front. Mol. Neurosci.

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Central nervous system (CNS) disorders, such as ischemic stroke, neurodegenerative diseases, multiple sclerosis, traumatic brain injury, and corresponding neuropathological changes, often lead to death or long-term disability. Long non-coding RNA (lncRNA) is a class of non-coding RNA with a transcription length over 200 nt and transcriptional regulation. lncRNA is extensively involved in physiological and pathological processes through epigenetic, transcription, and post-transcriptional regulation. Further, dysregulated lncRNA is closely related to the occurrence and development of human diseases, including CNS disorders. HOX Transcript antisense RNA (HOTAIR) is the first discovered lncRNA with trans-transcriptional regulation. Recent studies have shown that HOTAIR may participate in the regulation of the occurrence and development of CNS disorders. In addition, HOTAIR has the potential to become a new biomarker for the diagnosis and prognosis assessment of CNS disorders and even provide a new therapeutic target for CNS disorders. Here, we reviewed the research results of HOTAIR in CNS disorders to provide new insights into the pathogenesis, diagnostic value, and therapeutic target potential of HOTAIR in human CNS disorders.

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Aging, Cellular Senescence, and Alzheimer’s Disease

Cited by 80 publications

References 112 publications

Identification and Validation of Aging-Related Genes in Alzheimer’s Disease

Identification and Validation of Aging-Related Genes in Alzheimer’s Disease

Cellular Reprogramming and Its Potential Application in Alzheimer’s Disease

Long Non-coding RNA HOTAIR in Central Nervous System Disorders: New Insights in Pathogenesis, Diagnosis, and Therapeutic Potential

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