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Alzheimer’s disease (AD) is an insidiously progressive severe presenile and senile dementia, involving a number of cellular and biochemical mechanisms. AD affects millions of humans as the most common cause of cognitive decline worldwide, in addition to being a main medical challenge for aging population. From the clinical point of view, AD is mostly characterized by age-dependent inexorably progressing cognitive decline, affecting memory primarily associ‐ ated with behavioral and mood disorders, which increasingly appear as the disease advances [1]. From the neuropathological point of view, AD is mostly characterized by selective neuronal loss [2, 3], marked synaptic alterations [4–6], morphological mitochondrial abnor‐ malities [7, 8], tau pathology [9] resulting in neurofibrillary tangles (NFT) composed of hyperphosphorylated tau [10], inflammatory responses and by extracellular extensive deposits of polymers of Aβ peptide, in the form of neuritic plaques, which are a main hallmark of AD [11, 12]. These are dispersed in the neocortex, the hippocampus, and many subcortical structures, which play an important role in cognition. In addition, AD is characterized ultrastructurally by organelle pathology involving mostly the microtubules, the mitochondria, and Golgi apparatus [13].

Alterations of Mitochondria and Golgi Apparatus Are Related to Synaptic Pathology in Alzheimer's Disease