On the Common Journey of Neural Cells through Ischemic Brain Injury and Alzheimer’s Disease

Abstract

Ischemic brain injury and Alzheimer’s disease (AD) both lead to cell death in the central nervous system (CNS) and thus negatively affect particularly the elderly population. Due to the lack of a definitive cure for brain ischemia and AD, it is advisable to carefully study, compare, and contrast the mechanisms that trigger, and are involved in, both neuropathologies. A deeper understanding of these mechanisms may help ameliorate, or even prevent, the destructive effects of neurodegenerative disorders. In this review, we deal with ischemic damage and AD, with the main emphasis on the common properties of these CNS disorders. Importantly, we discuss the Wnt signaling pathway as a significant factor in the cell fate determination and cell survival in the diseased adult CNS. Finally, we summarize the interesting findings that may improve or complement the current sparse and insufficient treatments for brain ischemia and AD, and we delineate prospective directions in regenerative medicine.

Compromised Astrocyte Swelling/Volume Regulation in the Hippocampus of the Triple Transgenic Mouse Model of Alzheimer’s Disease

“…Although the disease has been intensively studied for more than a hundred years and several processes underlying neuronal loss have been proposed during this period, the overall understanding of the AD pathology remains incomplete. The most frequently declared causes of AD comprise neurodegeneration driven by amyloid-β (Aβ) toxicity and tau pathology, synaptic dysfunction as well as the loss of synaptic density, glutamate excitotoxicity, and oxidative stress (Smith et al, 2000;Hardy and Selkoe, 2002;Ingelsson et al, 2004;Walton and Dodd, 2007;Kriska et al, 2021). However, the pathological processes behind AD not only cause neuronal death, but also involve functional changes in other cell types, such as glia or pericytes, alterations in inter-cellular communication, changes in the composition of perineural networks, and vascular system disruption (De Strooper and Karran, 2016;Goetzl and Miller, 2017).…”

Gastrodin and Vascular Dementia: Advances and Current Perspectives

“…It is well known that microglia play a phagocytic role in the nervous system, and astrocytes can interact with microglia. Both of them jointly regulate inflammatory responses in the nervous system and play a key role in neuroinflammation and degenerative diseases [ 29 ]. Any nervous system disorder can lead to inflammation and activation of glial cells, which can lead to neuronal damage and ultimately cognitive deficits after ischemic hypoxia injury.…”

Crude Saponin from Platycodon grandiflorum Attenuates Aβ-Induced Neurotoxicity via Antioxidant, Anti-Inflammatory and Anti-Apoptotic Signaling Pathways

“…Alzheimer’s disease (AD) is a cognitive-behavioral disorder caused by degenerative changes in the cerebral cortex and hippocampal cells. The main pathological feature is the formation of senile plaques due to excessive accumulation of amyloid-beta (Aβ) [ 1 ]. In particular, the accumulation of Aβ induced by amyloid precursor protein (APP), which is highly neurotoxic, releases neurotoxic factors such as reactive oxygen species (ROS), proinflammatory cytokines, and chemokines, leading to neuronal damage.…”