scholarly journals Associations of the cerebrospinal fluid hepatocyte growth factor with Alzheimer’s disease pathology and cognitive function

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Li-Jing Zhao ◽  
Zuo-Teng Wang ◽  
Ya-Hui Ma ◽  
Wei Zhang ◽  
Qiang Dong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cognitive Decline ◽  
Regression Models ◽  
Linear Regression Models ◽  
Mediation Effects ◽  
Hepatocyte Growth

Abstract Background Hepatocyte growth factor (HGF) plays a role in neuronal survival and development, and has been implicated in neurodegenerative diseases. We sought to examine the associations of the CSF HGF with Alzheimer’s disease (AD) pathology and cognitive function. Methods A total of 238 participants (including 90 cognitively normal (CN) and 148 mild cognitive impairment (MCI)) who had measurements of CSF HGF were included from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. Multiple linear regression models were utilized to explore the cross-sectional associations of CSF HGF with AD biomarkers (including Aβ42, pTau, and tTau proteins) in non-demented participants. Moreover, linear mixed-effects regression models were utilized to explore the longitudinal associations of HGF subgroups with cognitive function. Mediation analyses were utilized to explore the mediation effects of AD markers. Results MCI individuals had significantly increased CSF HGF compared with the CN individuals. Results of multiple linear regressions showed significant correlations of CSF HGF with CSF Aβ42, pTau, and tTau in non-demented participants. Higher level of baseline CSF HGF was associated with faster cognitive decline. Influences of the baseline CSF HGF on cognition were partially mediated by Aβ42, pTau, and tTau pathologies. Conclusions High concentrations of HGF in CSF may be related to faster cognitive decline. The cognitive consequences of higher CSF HGF partly stem from AD pathology, which suggests that the CSF HGF may be an attractive biomarker candidate to track AD progression.

Hepatocyte growth factor (HGF/SF) in Alzheimer's disease

1998 ◽  
Vol 779 (1-2) ◽  
pp. 262-270 ◽  
Author(s):  
H Fenton ◽  
P.W Finch ◽  
J.S Rubin ◽  
J.M Rosenberg ◽  
W.G Taylor ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepatocyte Growth

scholarly journals Association of Sleep Disturbances and Cognitive Decline among Cognitively Normal Elders Over Time

2021 ◽  
Author(s):  
Wei Feng ◽  
Mandela William Nzoyoum Kuetche ◽  
Meng Zhang ◽  
MengMeng Liu ◽  
Deginet Aklilu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Regression Models ◽  
Sleep Disturbances ◽  
Amyloid Pet ◽  
Longitudinal Impact ◽  
Cognitively Normal ◽  
Over Time

Abstract Background: While sleep disturbances (SD) has been shown to be associated with worse cognition, but the causal relationship between the two subjects to debate. Our objective was to investigate the longitudinal impact of SD on cognitive function.Objective: To determine the effect of self-reported clinical diagnosis of SD on longitudinal changes in brain amyloid-PET, CSF-biomarkers (Aβ42, T-tau and P-tau) and cognitive function in cognitively normal.Methods: A total of 463 cognitively normal elders (357 normal and 106 SD) were included. Alzheimer’s Disease Neuroimaging Initiative (ADNI) participants were collected from 2005 to 2020. The generalized linear mixed models adjusting variables which were selected by the Akaike Information Criterion (AIC) and the marginal effect estimation method was used to estimate the risk effect of SD. Cox proportional hazards regression models estimated the relative hazard of Alzheimer’s Disease (AD), among baseline SD patients.Results: The age range of participants was 73.60±5.71 years old, and the female proportion was 43.63%. In adjusted regression models, Participants with baseline SD had higher likelihood of developing worse cognition over subsequent follow-up, PACC (decrease 7.53 points [95%CI, 7.36-7.70]; P<0.001), MMSE (decrease 5.26 points [95%CI, 5.17-5.35]; P<0.001), and CDR–Sum of Boxes (increase 5.61 points [95%CI, 5.67-5.54]; P=0.001). Similarly, Cox regression analysis suggested that sleep disturbances is a risk factor of AD (HR=1.55, 95% CI=1.08 to 2.22).Conclusion: SD probably is a warning sign of AD, because it is associated with greater likelihood of cognitive decline or dementia over time. Associations are likely multifactorial and could be explained by intervening variables in the path from SD to dementia, or by common risk factors for pathological processes in brain. These findings suggest need for more attentions of older adults with sleep compromise.

scholarly journals Hepatocyte Growth Factor in Synaptic Plasticity and Alzheimer's Disease

2010 ◽  
Vol 10 ◽  
pp. 457-461 ◽  
Author(s):  
Shiv K. Sharma
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Receptor Tyrosine Kinase ◽  
Hippocampal Neurons ◽  
Different Types ◽  
Hepatocyte Growth

The hepatocyte growth factor (HGF) was initially identified as a protein that promoted growth of hepatocytes. It regulates proliferation and survival of different types of cells. HGF signaling, which is initiated by its binding to a receptor tyrosine kinase, plays critical roles during development. HGF and its receptor are also present in brain cells. This review describes the role of HGF in hippocampal neurons, synaptic plasticity, and the memory impairment condition, Alzheimer's disease.

scholarly journals Moderating Effect of Insulin Resistance on the Relationship between Gray Matter Volumes and Cognitive Function

2018 ◽  
Vol 7 (11) ◽  
pp. 413 ◽  
Author(s):  
Jiyeon Lee ◽  
Jihyeon Kim ◽  
Seong Shin ◽  
Soowon Park ◽  
Dong Yoon ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Gray Matter ◽  
Structural Changes ◽  
Gray Matter Volume ◽  
Volume Loss ◽  
Matter Volume

Background: It is controversial whether exposure to insulin resistance accelerates cognitive deterioration. The present study aimed to investigate the association between insulin resistance and gray matter volume loss to predict the cognitive decline. Methods: We recruited 160 participants (78 with Alzheimer’s disease and 82 without Alzheimer’s disease). Insulin resistance, regional gray matter volume, and cognitive function were assessed. A hierarchical moderated multiple regression (MMR) model was used to determine any associations among insulin resistance, structural changes in the brain, and cognitive decline. Results: The volumes of 7 regions in the gray matter were negatively related to insulin resistance in Alzheimer’s disease (p =0.032). Hierarchical MMR analysis indicated that insulin resistance did not directly affect the cognitive decline but moderated the cognitive decline through the decrease in gray matter volume in the key brain regions, i.e., inferior orbitofrontal gyrus (left), middle cingulate gyrus (right), hippocampus (right), and precuneus (right) (p < 0.05 in each case). Conclusion: Insulin resistance appears to exacerbate the cognitive decline associated with several gray matter volume loss.

scholarly journals P-tau and neurodegeneration mediate the effect of β-amyloid on cognition in non-demented elders

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Ling-Zhi Ma ◽  
Hao Hu ◽  
Zuo-Teng Wang ◽  
Ya-Nan Ou ◽  
Qiang Dong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Mediating Effect ◽  
Total Effect ◽  
Independent Effect ◽  
Carrier Status ◽  
Mediation Effects ◽  
Β Amyloid ◽  
The Impact

Abstract Background There are many pathological changes in the brains of Alzheimer’s disease (AD) patients. For many years, the mainstream view on the pathogenesis of AD believes that β-amyloid (Aβ) usually acts independently in addition to triggering functions. However, the evidence now accumulating indicates another case that these pathological types have synergies. The objective of this study was to investigate whether effects of Aβ pathology on cognition were mediated by AD pathologies, including tau-related pathology (p-tau), neurodegeneration (t-tau, MRI measurements), axonal injury (NFL), synaptic dysfunction (neurogranin), and neuroinflammation (sTREM2, YKL-40). Methods Three hundred seventy normal controls (CN) and 623 MCI patients from the ADNI (Alzheimer’s Disease Neuroimaging Initiative) database were recruited in this research. Linear mixed-effects models were used to evaluate the associations of baseline Aβ with cognitive decline and biomarkers of several pathophysiological pathways. Causal mediation analyses with 10,000 bootstrapped iterations were conducted to explore the mediation effects of AD pathologies on cognition. Results Tau-related pathology, neurodegeneration, neuroinflammation are correlated with the concentration of Aβ, even in CN participants. The results show that age, gender, and APOE ε4 carrier status have a moderating influence on some of these relationships. There is a stronger association of Aβ with biomarkers and cognitive changes in the elderly and females. In CN group, Aβ pathology is directly related to poor cognition and has no mediating effect (p < 0.05). In mild cognitive impairment, tau-related pathology (26.15% of total effect) and neurodegeneration (14.8% to 47.0% of total effect) mediate the impact of Aβ on cognition. Conclusions In conclusion, early Aβ accumulation has an independent effect on cognitive decline in CN and a tau, neurodegeneration-dependent effect in the subsequent cognitive decline in MCI patients.

scholarly journals Effect of heterogeneity in patterns of cognitive function and dementia severity on cognitive decline in Alzheimer's disease

1999 ◽  
Vol 14 (1) ◽  
pp. 52-53
Author(s):  
C. M. Hooker ◽  
J. Szczepanik ◽  
M. L. Furey ◽  
P. Pietrini ◽  
M. J. Mentis ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Dementia Severity

scholarly journals Plasma Glutathione Levels Decreased with Cognitive Decline among People with Mild Cognitive Impairment (MCI): A Two-Year Prospective Study

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1839
Author(s):  
Chieh-Hsin Lin ◽  
Hsien-Yuan Lane
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Function ◽  
Prospective Study ◽  
Cognitive Decline ◽  
Cognitive Change ◽  
Disease Assessment ◽  
Healthy Individuals

Glutathione (GSH) is a major endogenous antioxidant. Several studies have shown GSH redox imbalance and altered GSH levels in Alzheimer’s disease (AD) patients. Early detection is crucial for the outcome of AD. However, whether GSH can serve as a biomarker during the very early-phase of AD, such as mild cognitive impairment (MCI), remains unknown. The current prospective study aimed to examine the longitudinal change in plasma GSH concentration and its influence on cognitive decline in MCI. Overall, 49 patients with MCI and 16 healthy individuals were recruited. Plasma GSH levels and cognitive function, measured by the Mini-Mental Status Examination (MMSE) and Alzheimer’s disease assessment scale-cognitive subscale (ADAS-cog), were monitored every 6 months. We employed multiple regressions to examine the role of GSH level in cognitive decline in the 2 years period. The MCI patients showed significant decline in plasma GSH levels and cognitive function from baseline to endpoint (month 24). In comparison, the healthy individuals’ GSH concentration and cognitive function did not change significantly. Further, both GSH level at baseline and GSH level change from baseline to endpoint significantly influenced cognitive decline among the MCI patients. To our knowledge, this is the first study to demonstrate that both plasma GSH levels and cognitive function declined 2 years later among the MCI patients in a prospective manner. If replicated by future studies, blood GSH concentration may be regarded as a biomarker for monitoring cognitive change in MCI.

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