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Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by memory loss and multiple cognitive impairments. Several decades of intensive research have shown that multicellular changes are involved in AD’s development and progression, including mitochondrial damage, synaptic dysfunction, formation and accumulation of beta-amyloid (Aβ), formation and accumulation of hyperphosphorylated tau protein, and loss of neurons in patients with this disease. Among them, mitochondrial dysfunction and synaptic damage are the primary manifestations in the disease process. Recent studies have also shown that defective mitophagy caused by Aβ and tau protein are the main indicators in AD’s pathogenesis. This review includes an overview of recent researches on the role of mitochondria in AD development. The review summarizes several aspects of mitochondrial dysfunction, including abnormal mitochondrial dynamics, changes in mitochondrial DNA, and calcium dyshomeostasis in AD pathogenesis

Alzheimer’s disease (AD) is the most common type of dementia and is characterized by accumulating amyloid (Aβ) plaques and neurofibrillary tangles in the brain. Excessive stimulation of glutamate receptors, mainly NMDA-type, causes intense entry of calcium ions into cells and is a key early step in glutamateinduced excitotoxicity, resulting in many neurological diseases, including AD. Memantine, an NMDA receptor antagonist, blocks NMDA receptors and reduce the influx of calcium ions into neuron. In our experiments, we have modeled AD on cultured rat hippocampal neurons to test the effects of memantine on calcium signaling in neurons. Our results show that the neuroprotective effect of memantine could be provided not only through the inhibition of NMDA receptor current but also through the suppression of voltage-dependent Ca2+ channels, most likely L-type. This study suggests that NMDA receptor antagonist memantine can protect hippocampal neurons from calcium overloading induced by Aβ1–42 amyloid exposure via blocking Ca2+ channels

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