Astrocyte Senescence and Alzheimer’s Disease: A Review

Han, Xiaobin; Zhang, Tianying; Liu, Huanhuan; Mi, Yajing; Gou, Xin

doi:10.3389/fnagi.2020.00148

Cited by 95 publications

(94 citation statements)

References 148 publications

(237 reference statements)

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“…In this study, we found that: (1) WT and AD mice showed different correlation patterns between Hip/PFC EEG activity and behavioral memory; (2) based on regression correlations, treatment with the GABA A antagonist bicuculline improved brain function in AD mice, but resulted in poorer brain function in WT mice; (3) treatment with the GABA A agonist muscimol benefited AD mice, but showed no obvious effects on WT mice.…”

Section: Discussionmentioning

confidence: 80%

“…At present, the incidence of AD is 4% among individuals aged 65 and up to 40%-50% among individuals aged 85 (1,2). Evidence suggests that brain senescence contributes to AD pathogenesis (3,4), and a link exists between the aging process and disease development (5)(6)(7). As aging is an important risk factor for AD, it would be interesting to compare differences between AD and normal aging, and thus help clarify the neural mechanisms of AD.…”

Section: Introductionmentioning

confidence: 99%

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Different correlation patterns between EEG and memory after E/I balance adjustment in normal middle-aged mice and AD model mice

Zheng

2020

Preprint

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Alzheimer’s disease (AD) is correlated with brain atrophy, neuronal loss, neurotransmitter imbalance, and cognitive decline, which also occur in normal aging. Thus, comparing the differences between normal aging and AD is of interest in order to test the accelerated aging hypothesis of AD. An imbalance between excitatory/inhibitory (E/I) neurotransmission, especially in gamma-aminobutyric acid (GABA) inhibition dysfunction, is involved in both AD and normal aging. In the present study, we performed correlation analyses between electroencephalograms (EEGs) and memory in middle-aged (∼12 months old) wild-type mice (WT) and AD model mice (APP/PS1) after E/I balance adjustment via GABAA agonist muscimol and antagonist bicuculline administration (0.1 mg/kg intraperitoneally). Specifically, EEGs of the hippocampus and prefrontal cortex were recorded during Y-maze performance. Overall, WT and AD mice showed different correlation patterns between EEG activity and behavioral memory performance. Significant correlations were observed in EEG activity across a wider range of frequency bands (2–100 Hz, except 4–8 Hz) in WT mice, but were mainly observed in low frequency bands (delta-theta, 2–8 Hz) in AD mice. In addition, muscimol and bicuculline treatment contributed to better brain function in AD mice; in contrast, bicuculline administration resulted in poorer brain function in WT mice. Thus, our study suggests that AD shows a distinct pattern of disrupted brain function, rather than accelerated aging. Importantly, this work reveals new insights into future AD treatment by influencing low-frequency EEG activity through E/I balance adjustment, thereby aiding cognitive recovery.

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Section: Discussionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Different correlation patterns between EEG and memory after E/I balance adjustment in normal middle-aged mice and AD model mice

Zheng

2020

Preprint

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“…This reduction in glial glutamate uptake capacity in SAMP8 may elevate extracellular glutamate levels, leading to neuronal excitotoxicity [ 85 ], and contribute to premature learning and memory deficits observed not only in this murine model of early aging but also of AD. In fact, astrocyte senescence and its putative role in the pathologic progress of AD has been recently reviewed [ 86 ]. Astrocytes cultured from neonatal SAMP8 mice present similar alterations to those described in the whole brains of SAMP8 mice at 1–5 months of age [ 83 ].…”

Section: Discussionmentioning

confidence: 99%

Adenosine Metabolism in the Cerebral Cortex from Several Mice Models during Aging

Sánchez-Melgar

Albasanz

Pallàs

et al. 2020

IJMS

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Adenosine is a neuromodulator that has been involved in aging and neurodegenerative diseases as Alzheimer’s disease (AD). In the present work, we analyzed the possible modulation of purine metabolites, 5’nucleotidase (5′NT) and adenosine deaminase (ADA) activities, and adenosine monophosphate (AMP)-activated protein kinase (AMPK) and its phosphorylated form during aging in the cerebral cortex. Three murine models were used: senescence-accelerated mouse-resistant 1 (SAMR1, normal senescence), senescence-accelerated mouse-prone 8 (SAMP8, a model of AD), and the wild-type C57BL/6J (model of aging) mice strains. Glutamate and excitatory amino acid transporter 2 (EAAT2) levels were also measured in these animals. HPLC, Western blotting, and enzymatic activity evaluation were performed to this aim. 5′-Nucleotidase (5′NT) activity was decreased at six months and recovered at 12 months in SAMP8 while opposite effects were observed in SAMR1 at the same age, and no changes in C57BL/6J mice. ADA activity significantly decreased from 3 to 12 months in the SAMR1 mice strain, while a significant decrease from 6 to 12 months was observed in the SAMP8 mice strain. Regarding purine metabolites, xanthine and guanosine levels were increased at six months in SAMR1 without significant differences in SAMP8 mice. In C57BL/6J mice, inosine and xanthine were increased, while adenosine decreased, from 4 to 24 months. The AMPK level was decreased at six months in SAMP8 without significant changes nor in SAMR1 or C57BL/6J strains. Glutamate and EAAT2 levels were also modulated during aging. Our data show a different modulation of adenosine metabolism participants in the cerebral cortex of these animal models. Interestingly, the main differences between SAMR1 and SAMP8 mice were found at six months of age, SAMP8 being the most affected strain. As SAMP8 is an AD model, results suggest that adenosinergic metabolism is involved in the neurodegeneration of AD.

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“…Positron emission tomographic amyloid imaging, cerebrospinal fluid tau and Aβ levels have high specificity in the diagnosis of AD. 5 However, they are expensive and timeconsuming.…”

Section: Introductionmentioning

confidence: 99%

<p>Evaluation of Retinal Nerve Fiber Layer and Ganglion Cell Layer Thickness in Alzheimer’s Disease Using Optical Coherence Tomography</p>

Jindahra¹,

Hengsiri²,

Witoonpanich³

et al. 2020

OPTH

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Objective: To evaluate the feasibility of using optical coherence tomography (OCT) for the detection of Alzheimer's disease (AD), by measuring the thickness of the retinal nerve fiber layer (RNFL) and the ganglion cell layer and inner plexiform layer (GCL-IPL). Material and Methods: This was a single-center, cross-sectional study. The study included 29 patients with AD (mean age ± standard deviation: 75.61 ± 6.24 years) and 29 healthy age-and sex-matched controls. All participants underwent cognitive evaluations using the Montreal Cognitive Assessment test. Measurements of the RNFL thickness, as well as GCL-IPL thickness, were obtained for all participants using OCT. Both RNFL and GCL-IPL parameters were adjusted for best-corrected visual acuity, hypertension, diabetes and dyslipidemia. Results: The mean RNFL thickness was significantly thinner in the AD group than in the control group (85.24 and 90.68 µm, respectively, adjusted P=0.014). The superior quadrant was thinner in the AD group (adjusted P=0.033). The thicknesses did not differ significantly between groups for the other quadrants. The mean GCL-IPL thickness in the AD (68.81 µm) was significantly thinner than that in the controls (76.42 µm) (adjusted P=0.014). Overall, there was a negative correlation between age and mean RNFL; and between age and GCL-IPL thickness (r=−0.338, P=0.010 and r=−0.346, P=0.008, respectively). Conclusion: The mean RNFL and GCL-IPL thicknesses were thinner in the AD group than in the control group. These findings suggest that RNFL and GCL-IPL thickness may be biological markers for AD.

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Astrocyte Senescence and Alzheimer’s Disease: A Review

Cited by 95 publications

References 148 publications

Different correlation patterns between EEG and memory after E/I balance adjustment in normal middle-aged mice and AD model mice

Different correlation patterns between EEG and memory after E/I balance adjustment in normal middle-aged mice and AD model mice

Adenosine Metabolism in the Cerebral Cortex from Several Mice Models during Aging

<p>Evaluation of Retinal Nerve Fiber Layer and Ganglion Cell Layer Thickness in Alzheimer’s Disease Using Optical Coherence Tomography</p>

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