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

John C. Gant; Inga Kadish; Kuey Chu Chen; Olivier Thibault; Eric M. Blalock; Nada M. Porter; Philip W. Landfield

doi:10.3233/JAD-180618

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

John C. Gant
, Inga Kadish
, Kuey Chu Chen
, Olivier Thibault
, Eric M. Blalock
, Nada M. Porter
, Philip W. Landfield

Pharmacology and Nutritional Sciences

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

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 Ca 2 + 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 Ca 2 + dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.

Original language	English
Pages (from-to)	1371-1378
Number of pages	8
Journal	Journal of Alzheimer's Disease
Volume	66
Issue number	4
DOIs	https://doi.org/10.3233/JAD-180618
State	Published - 2018

Bibliographical note

Publisher Copyright:
© 2018 - IOS Press and the authors. All rights reserved.

Funding

This work was supported by NIH grants AG004542, AG052050, and AG037868.

Funders	Funder number
National Institutes of Health (NIH)	AG004542, AG037868
National Institute on Aging	R21AG052050

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Afterhyperpolarization
FKBP
aging models
calcium-dependent
cytoskeleton
hippocampus
neurofibrillary progression
ryanodine receptor

ASJC Scopus subject areas

General Neuroscience
Clinical Psychology
Geriatrics and Gerontology
Psychiatry and Mental health

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10.3233/JAD-180618

Cite this

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

abstract = "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 Ca 2 + 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 Ca 2 + dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.",

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AU - Gant, John C.

AU - Kadish, Inga

AU - Chen, Kuey Chu

AU - Thibault, Olivier

AU - Blalock, Eric M.

AU - Porter, Nada M.

AU - Landfield, Philip W.

PY - 2018

Y1 - 2018

N2 - 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 Ca 2 + 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 Ca 2 + dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.

AB - 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 Ca 2 + 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 Ca 2 + dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.

KW - Afterhyperpolarization

KW - FKBP

KW - aging models

KW - calcium-dependent

KW - cytoskeleton

KW - hippocampus

KW - neurofibrillary progression

KW - ryanodine receptor

UR - https://www.scopus.com/pages/publications/85058787266

UR - https://www.scopus.com/pages/publications/85058787266#tab=citedBy

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DO - 10.3233/JAD-180618

M3 - Article

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AN - SCOPUS:85058787266

SN - 1387-2877

VL - 66

SP - 1371

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JO - Journal of Alzheimer's Disease

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ER -

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

Abstract

Bibliographical note

Funding

UN SDGs

Keywords

ASJC Scopus subject areas

Access to Document

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