Aging-Related Calcium Dysregulation in Rat Entorhinal Neurons Homologous with the Human Entorhinal Neurons in which Alzheimer's Disease Neurofibrillary Tangles First Appear

被引：7

作者：

Gant, John C. ^{[1
]}

Kadish, Inga ^{[2
]}

Chen, Kuey-Chu ^{[1
]}

Thibault, Olivier ^{[1
]}

Blalock, Eric M. ^{[1
]}

Porter, Nada M. ^{[1
]}

Landfield, Philip W. ^{[1
]}

机构：

[1] Univ Kentucky, Dept Pharmacol & Nutr Sci, 800 Rose St,UKMC MS 307, Lexington, KY 40536 USA

[2] Univ Alabama Birmingham, Dept Cell Dev & Integrat Biol, Birmingham, AL USA

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2018年 / 66卷 / 04期

关键词：

Afterhyperpolarization; aging models; calcium-dependent; cytoskeleton; FKBP; hippocampus; neurofibrillary progression; ryanodine receptor; FK506-BINDING PROTEIN 12.6/1B; ANIMAL-MODELS; HIPPOCAMPAL-NEURONS; DENTATE GYRUS; MOUSE MODEL; CORTEX; BRAIN; CELLS; CA2+; PROJECTIONS;

D O I：

10.3233/JAD-180618

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Aging is the leading risk factor for idiopathic Alzheimer's disease (AD), indicating that normal aging processes promote AD and likely are present in the neurons in which AD pathogenesis originates. In AD, neurofibrillary tangles (NFTs) appear first in entorhinal cortex, implying that aging processes in entorhinal neurons promote NFT pathogenesis. Using electrophysiology and immunohistochemistry, we find pronounced aging-related Ca2+ dysregulation in rat entorhinal neurons homologous with the human neurons in which NFTs originate. Considering that humans recapitulate many aspects of animal brain aging, these results support the hypothesis that aging-related Ca2+ dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.

引用

页码：1371 / 1378

页数：8