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International Journal of Physiology and Pathophysiology
SJR: 0.116

ISSN Imprimir: 2155-014X
ISSN On-line: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v1.i3.100
pages 287-304

Molecular and Cellular Mechanisms of Alzheimer's Disease Development

Elena P. Kostyuk
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Tatyana Yu. Korol
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Platon G. Kostyuk
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv

RESUMO

Neuropathological studies classified several neurodegenerative illnesses among which Alzheimer's and Parkinson diseases are the most frequent. Alzheimer's disease is characterized by the presence of cognitive syndromes and almost completes destruction of memory. It is suggested that the basis of these syndromes is an elevation of the amount of β-amyloid-42 protein (mainly in hippocampal neurons), changes in calcium homeostasis and synaptic plasticity. Recent data indicate that alterations of calcium homeostasis connected with changes in neuronal membrane and functioning of the endoplasmic reticulum, leading to long − lasting alterations synaptic potenthiation and depression. Therefore the task of this review was the analysis of alterations in the functioning of structures involved in calcium homeostasis, including mitochondria, calcium channels, processes leading to changes in synaptic plasticity. Beside this we wanted to decide which process are the leading ones in the development of Alzheimer's disease − accumulation in hippocampal neurons and dendrites of β-amyloid or alteration in calcium homeostasis (mainly from the data of literature).


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