The Early Events That Initiate β-Amyloid Aggregation in Alzheimer’s Disease

Zhang, Xingyu; Fu, Zhihui; Meng, Lanxia; He, Mingyang; Zhang, Zhentao

doi:10.3389/fnagi.2018.00359

Cited by 98 publications

(80 citation statements)

References 213 publications

(237 reference statements)

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“…Although the cause of AD remains unclear, Aβ accumulation in the brain was proposed to play a major role in the onset of this disease [35,36]. Partial reproduction of AD neuropathological conditions and cognitive deficits can be achieved with pharmacological drug-induced approaches Evidence-Based Complementary and Alternative Medicine and Aβ overexpression [37].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Ooi

Munawar

Rosli

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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This study aimed to determine the effects of tropical fruit juice mixture (pomegranate, white guava, and Roselle) on biochemical, behavioral, and histopathological changes of β-amyloid- (Aβ-) induced rats. Formulation 8 (F8) of tropical fruit juice mixture was chosen for this present study due to its high phenolic content and antioxidant capacity. Forty Wistar male rats were divided into five groups: dPBS (sham-operated control), dAβ (Aβ control), JPBS (F8 and PBS), JAβ (F8 and Aβ), and IBFAβ (ibuprofen and Aβ). F8 (5 ml/kg BW), and ibuprofen (10 ml/kg BW) was given orally daily for four weeks before the intracerebroventricular infusion of Aβ for two weeks. Histological analysis and neuronal count of hippocampus tissue in the Cornu Ammonis (CA1) region showed that supplementation with F8 was able to prevent Aβ-induced tissue damage and neuronal shrinkage. However, no significant difference in locomotor activity and novel object recognition (NOR) percentage was detected among different groups at day 7 and day 14 following Aβ infusion. Only effect of time differences (main effect of day) was observed at day 7 as compared to day 14, where reduction in locomotor activity and NOR percentage was observed in all groups, with F (1, 7) = 6.940, p<0.05 and F (1, 7) = 7.152, p<0.05, respectively. Besides, the MDA level of the JAβ group was significantly lower (p<0.01) than that of the dPBS group. However, no significant changes in SOD activity were detected among different groups. Significant reduction in plasma CRH level (p<0.05) and iNOS expression (p<0.01) in the brain was detected in the JAβ group as compared to the dAβ group. Hence, our current findings suggest that the tropical fruit juice mixture (F8) has the potential to protect the rats from Aβ-induced neurotoxicity in brain hippocampus tissue possibly via its antioxidant properties and the suppression of iNOS expression and CRH production.

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Section: Discussionmentioning

confidence: 99%

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Ooi

Munawar

Rosli

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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“…AD is pathologically characterized by the accumulation of amyloid-beta (Aβ) plaques, tau neurofibrillary tangles (NFTs), synaptic and neuronal loss, glial activation, and neuroinflammation [6][7][8][9][10][11]. Aβ plaques and NFTs induce an immune response associated with astroglia and microglia activation and increased inflammatory mediators, tumor necrosis factor α [12], S100, interleukin 1 [13,14], such as triggering receptor expressed on myeloid cells 2 (TREM2) [15,16], and complement activation (C1q to C5b-9) [17] in AD [18][19][20]. Recently, the chitinase family of inflammatory proteins, particularly chitinase 3-like 1 (CHI3L1, YKL-40, or HC gp-39), chitinase 3-like 2 (CHI3L2 or YKL- 39), and pentraxin II (NPTX2 or Narp), a member of the pentraxin family, has been associated with AD pathogenesis [21,22].…”

Section: Introductionmentioning

confidence: 99%

Frontal cortex chitinase and pentraxin neuroinflammatory alterations during the progression of Alzheimer’s disease

Moreno‐Rodríguez

Perez

Nadeem

et al. 2020

J Neuroinflammation

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Background: Chitinase 3-like 1 (CHI3L1), chitinase 3-like 2 (CHI3L2), and neuronal pentraxin II (NPTX2) are inflammatory biomarkers of Alzheimer's disease (AD). Although studies have demonstrated that cerebrospinal fluid levels of these proteins are changed in AD, no studies have undertaken a detailed examination of alterations in protein levels, cellular expression, and interaction with amyloid in the brain during the progression of AD. Methods:The study evaluated levels of both CHI3L1 and CHI3L2, NPTX2, ionized calcium-binding adapter molecule 1 (Iba1), complement component 1q (C1q), glial fibrillary acidic protein (GFAP), and CD44, in the frontal cortex of people who died with an antemortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI), mild/moderate AD (mAD), and severe AD (sAD) using immunoblot and immunohistochemical techniques.Results: CHI3L1-immunoreactive (-ir) astrocyte numbers were increased in the frontal cortex and white matter in sAD compared to NCI. On the other hand, increases in GFAP and Iba1-ir cell numbers were observed in MCI compared to NCI but only in white matter. Western blot analyses revealed significantly lower frontal cortex CHI3L2 levels, whereas CD44 levels were increased in sAD. No significant differences for CHI3L1, GFAP, C1q, and NPTX2 protein levels were detected between clinical groups. Strong significant correlations were found between frontal cortex CHI3L1 and Iba1-ir cell numbers in white matter and CHI3L1 and C1q protein levels in the early stages of the disease. C1q and Iba1, CD44 with CHI3L2, and GFAP protein levels were associated during disease progression. CHI3L1 and Iba1 cell numbers in white matter showed a significant associations with episodic memory and perceptual speed.Conclusions: White matter CHI3L1 inflammatory response is associated with cognitive impairment early in the onset of AD.

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“…In the prospective cohort study, serum glucose, insulin, and HOMA values and postmortem AD pathology were assessed. After statistical analysis using analysis of variance and a continuous analysis with linear mixed models It was found no association between lifetime measures of glucose homeostasis and standard measures of AD pathology or cortical fibrillary Aβ deposition [29].…”

Section: Brain Energy Metabolism and Ad Onsetmentioning

confidence: 88%

“…Correct insulin signaling provides a physiological defense mechanism against the toxic effects of Aβ oligomers on synapses by reducing oligomer binding sites in neurons. Insulin has multiple anti-amyloidogenic effects on human nerve cells, including preventing the translocation of an intracellular domain fragment of the amyloid precursor protein (APP) into the nucleus, increasing the transcription of anti-amyloidogenic proteins and increasing the α-secretase-dependent APP processing pathway [29].…”

Section: Insulin Role In the Brainmentioning

confidence: 99%

“…In addition to the effect of S100B on RAGE-mediated ROS overproduction, this protein, at concentrations of ≥500 nM, enhances Aβ neurotoxicity. However, at lower concentrations, S100B showed a protective effect against the neurotoxicity of Aβ [25][26][27][28][29][30][31][32][33][34][35] [101]. Furthermore, recent studies suggested that elevated S100B levels have harmful effects on oligodendrogenesis and myelination through RAGE-dependent processes.…”

Section: S100 Protein Family As a Potential Biomarkers Of Admentioning

confidence: 99%

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The Interplay between Diabetes and Alzheimer’s Disease—In the Hunt for Biomarkers

Kubis-Kubiak

Dyba

Piwowar

2020

IJMS

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The brain is an organ in which energy metabolism occurs most intensively and glucose is an essential and dominant energy substrate. There have been many studies in recent years suggesting a close relationship between type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) as they have many pathophysiological features in common. The condition of hyperglycemia exposes brain cells to the detrimental effects of glucose, increasing protein glycation and is the cause of different non-psychiatric complications. Numerous observational studies show that not only hyperglycemia but also blood glucose levels near lower fasting limits (72 to 99 mg/dL) increase the incidence of AD, regardless of whether T2DM will develop in the future. As the comorbidity of these diseases and earlier development of AD in T2DM sufferers exist, new AD biomarkers are being sought for etiopathogenetic changes associated with early neurodegenerative processes as a result of carbohydrate disorders. The S100B protein seem to be interesting in this respect as it may be a potential candidate, especially important in early diagnostics of these diseases, given that it plays a role in both carbohydrate metabolism disorders and neurodegenerative processes. It is therefore necessary to clarify the relationship between the concentration of the S100B protein and glucose and insulin levels. This paper draws attention to a valuable research objective that may in the future contribute to a better diagnosis of early neurodegenerative changes, in particular in subjects with T2DM and may be a good basis for planning experiments related to this issue as well as a more detailed explanation of the relationship between the neuropathological disturbances and changes of glucose and insulin concentrations in the brain.

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The Early Events That Initiate β-Amyloid Aggregation in Alzheimer’s Disease

Cited by 98 publications

References 213 publications

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Frontal cortex chitinase and pentraxin neuroinflammatory alterations during the progression of Alzheimer’s disease

The Interplay between Diabetes and Alzheimer’s Disease—In the Hunt for Biomarkers

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