TUNEL and growth factor expression in the prefrontal cortex of Alzheimer patients over 80 years old.

Standard

TUNEL and growth factor expression in the prefrontal cortex of Alzheimer patients over 80 years old. / Lorke, Dietrich; Wai, M S M; Liang, Y; Yew, D T.

in: INT J IMMUNOPATH PH, Jahrgang 23, Nr. 1, 1, 2010, S. 13-23.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

APA

Vancouver

Lorke D, Wai MSM, Liang Y, Yew DT. TUNEL and growth factor expression in the prefrontal cortex of Alzheimer patients over 80 years old. INT J IMMUNOPATH PH. 2010;23(1):13-23. 1.

Bibtex

@article{d4065d20220d427e9a7b7bf0b53cad60,
title = "TUNEL and growth factor expression in the prefrontal cortex of Alzheimer patients over 80 years old.",
abstract = "To elucidate factors underlying the increased risk of developing Alzheimers disease (AD) in older individuals, the prefrontal cortices of younger (58-79 years) and of older (over 80 years) AD patients were examined by silver impregnation, TUNEL assay and immunohistochemistry for hyperphosphorylated tau, LDH and two growth factors (BDNF, NGF). Quantitative data were compared with those of age-matched controls. TUNEL-positive cells were mainly located in superficial cortical layers of younger and in deeper layers of older AD patients. Their density was more than 5 times higher in older AD than in younger AD (p <or = 0.05), but apoptotic cell morphology was rarely seen. Significantly more neuronal somas were contacted by degenerating fibers both in younger and older AD cortices. Density of tau-immunoreactive cells, which were virtually absent in controls, was twice as high in older AD patients as in younger AD individuals (p <or = 0.05). In younger AD, TUNEL positive cells generally lacked tau immunoreaction, whereas in older AD, most cells were double-labeled for hyperphosphorylated tau and TUNEL (p <or = 0.05). Numerical density of BDNF-immunoreactive cells was significantly reduced by 20 percent in older AD patients, compared to both control individuals and younger AD patients, whereas density of NGF-positive cells was the same in all patient groups examined. The distinct differences between younger and older AD patients suggest a faster progression of AD in older patients.",
keywords = "Humans, Male, Aged, Female, Middle Aged, Aged, 80 and over, Phosphorylation, Alzheimer Disease metabolism, Brain-Derived Neurotrophic Factor analysis, In Situ Nick-End Labeling, L-Lactate Dehydrogenase analysis, Nerve Growth Factor analysis, Prefrontal Cortex chemistry, tau Proteins metabolism, Humans, Male, Aged, Female, Middle Aged, Aged, 80 and over, Phosphorylation, Alzheimer Disease metabolism, Brain-Derived Neurotrophic Factor analysis, In Situ Nick-End Labeling, L-Lactate Dehydrogenase analysis, Nerve Growth Factor analysis, Prefrontal Cortex chemistry, tau Proteins metabolism",
author = "Dietrich Lorke and Wai, {M S M} and Y Liang and Yew, {D T}",
year = "2010",
language = "Deutsch",
volume = "23",
pages = "13--23",
number = "1",

}

RIS

TY - JOUR

T1 - TUNEL and growth factor expression in the prefrontal cortex of Alzheimer patients over 80 years old.

AU - Lorke, Dietrich

AU - Wai, M S M

AU - Liang, Y

AU - Yew, D T

PY - 2010

Y1 - 2010

N2 - To elucidate factors underlying the increased risk of developing Alzheimers disease (AD) in older individuals, the prefrontal cortices of younger (58-79 years) and of older (over 80 years) AD patients were examined by silver impregnation, TUNEL assay and immunohistochemistry for hyperphosphorylated tau, LDH and two growth factors (BDNF, NGF). Quantitative data were compared with those of age-matched controls. TUNEL-positive cells were mainly located in superficial cortical layers of younger and in deeper layers of older AD patients. Their density was more than 5 times higher in older AD than in younger AD (p <or = 0.05), but apoptotic cell morphology was rarely seen. Significantly more neuronal somas were contacted by degenerating fibers both in younger and older AD cortices. Density of tau-immunoreactive cells, which were virtually absent in controls, was twice as high in older AD patients as in younger AD individuals (p <or = 0.05). In younger AD, TUNEL positive cells generally lacked tau immunoreaction, whereas in older AD, most cells were double-labeled for hyperphosphorylated tau and TUNEL (p <or = 0.05). Numerical density of BDNF-immunoreactive cells was significantly reduced by 20 percent in older AD patients, compared to both control individuals and younger AD patients, whereas density of NGF-positive cells was the same in all patient groups examined. The distinct differences between younger and older AD patients suggest a faster progression of AD in older patients.

AB - To elucidate factors underlying the increased risk of developing Alzheimers disease (AD) in older individuals, the prefrontal cortices of younger (58-79 years) and of older (over 80 years) AD patients were examined by silver impregnation, TUNEL assay and immunohistochemistry for hyperphosphorylated tau, LDH and two growth factors (BDNF, NGF). Quantitative data were compared with those of age-matched controls. TUNEL-positive cells were mainly located in superficial cortical layers of younger and in deeper layers of older AD patients. Their density was more than 5 times higher in older AD than in younger AD (p <or = 0.05), but apoptotic cell morphology was rarely seen. Significantly more neuronal somas were contacted by degenerating fibers both in younger and older AD cortices. Density of tau-immunoreactive cells, which were virtually absent in controls, was twice as high in older AD patients as in younger AD individuals (p <or = 0.05). In younger AD, TUNEL positive cells generally lacked tau immunoreaction, whereas in older AD, most cells were double-labeled for hyperphosphorylated tau and TUNEL (p <or = 0.05). Numerical density of BDNF-immunoreactive cells was significantly reduced by 20 percent in older AD patients, compared to both control individuals and younger AD patients, whereas density of NGF-positive cells was the same in all patient groups examined. The distinct differences between younger and older AD patients suggest a faster progression of AD in older patients.

KW - Humans

KW - Male

KW - Aged

KW - Female

KW - Middle Aged

KW - Aged, 80 and over

KW - Phosphorylation

KW - Alzheimer Disease metabolism

KW - Brain-Derived Neurotrophic Factor analysis

KW - In Situ Nick-End Labeling

KW - L-Lactate Dehydrogenase analysis

KW - Nerve Growth Factor analysis

KW - Prefrontal Cortex chemistry

KW - tau Proteins metabolism

KW - Humans

KW - Male

KW - Aged

KW - Female

KW - Middle Aged

KW - Aged, 80 and over

KW - Phosphorylation

KW - Alzheimer Disease metabolism

KW - Brain-Derived Neurotrophic Factor analysis

KW - In Situ Nick-End Labeling

KW - L-Lactate Dehydrogenase analysis

KW - Nerve Growth Factor analysis

KW - Prefrontal Cortex chemistry

KW - tau Proteins metabolism

M3 - SCORING: Zeitschriftenaufsatz

VL - 23

SP - 13

EP - 23

IS - 1

M1 - 1

ER -