What is it about?
Electron microscopy enlarged the horizons of morphological investigation in AD and revealed dendritic, spine and marked synaptic pathology, in association with substantial organelle alterations, involving mostly microtubules, mitochondria , Golgi apparatus (GA) and endoplasmic reticulum (ER) clearly observed even in areas of the brain, where dendritic plaques and neurofibrillary tangles are infrequent.
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Why is it important?
The alterations of ER and GA result in accumulation of misfolded proteins and neuronal loss, given that failure of the adaptive mechanisms of the unfolded protein response (UPR) may result in chronic accumulation of misfolded proteins in theER and impaired amyloid precursor protein (APP) processing and trafficking.In addition Tau protein, which is accumulated in ER, Golgi complexes, and mitochondria , may activate the unfolded protein response by impairing ER-associated degradation . In addition all newly synthesized proteins, which are used for membranic processes, insertion or secretion, axoplasmic or dendritic flow and synaptic activity, including APP, are practically processed through the vesicles and the cisternae of Golgi complex.The GA in the majority of the early cases of AD is fragmented and atrophic in comparison with age matched normal controls. The number of the vacuoles and vesicles, which are associated with the Golgi complex, are reduced in most of the Purkinje and granule cells of the cerebellum, the hippocampal neurons, the acoustic and visual cortices as well as the hypothalamus . It must be emphasized that alterations of GA are also observed in the astrocytes, in endothelial cells as well as in pericytes in AD brains .
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This page is a summary of: Golgi apparatus in Alzheimer’s disease, Journal of Neurology & Stroke, June 2015, MedCrave Group LLC,
DOI: 10.15406/jnsk.2015.02.00056.
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