Analytical Review on Normal Brain Aging, Alzheimer’s Disease, and Stage 4S Neuroblastoma: Novel Insights Into Neuroprotection, Neurodegeneration, and Spontaneous Regression
Nevim Aygun
TL;DR
This review explores brain aging, Alzheimer's disease, and stage 4S neuroblastoma, highlighting shared mechanisms like autophagy and apoptosis.
Contribution
The paper provides novel insights into the molecular links between neurodegeneration and spontaneous tumor regression.
Findings
PRH1 and MIR181A1HG may offer neuroprotection in elderly females' brains.
Impaired autophagy and apoptosis are key in both Alzheimer's and stage 4S neuroblastoma.
Loss of oligodendrocytes and reduced neurogenesis contribute to cognitive decline in Alzheimer's.
Abstract
The normal aging brain does not show massive neuron loss. However, neurodegenerative diseases are characterized by the progressive loss of neurons that differentiate from neuroblasts arising in the neural tube. Oxidative stress induces protein misfolding and aggregation that generates endoplasmic reticulum (ER) stress, leading to the activation of the unfolded protein response (UPR). Oxidative stress can also impair autophagy and mitophagy. Prolonged ER stress and impaired autophagy or mitophagy together can promote neuronal death. Neuroblastoma is an embryonal tumor developing from sympathetic neuroblasts. Stage 4S neuroblastoma is frequently associated with spontaneous regression. Autophagy decreases in stage 4S neuroblastoma, whereas apoptosis increases. The present review focuses on the molecular and cellular fundamentals of normal brain aging, neurodegenerative diseases, and…
Genes, proteins, chemicals, diseases, species, mutations and cell lines named across the full text — each resolved to its canonical identifier and authoritative record.
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Taxonomy
TopicsAlzheimer's disease research and treatments · Genetics and Neurodevelopmental Disorders · Mitochondrial Function and Pathology