scholarly journals Coffee intake and decreased amyloid pathology in human brain

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jee Wook Kim ◽  
◽  
Min Soo Byun ◽  
Dahyun Yi ◽  
Jun Ho Lee ◽  
...  

Abstract Several epidemiological and preclinical studies supported the protective effect of coffee on Alzheimer’s disease (AD). However, it is still unknown whether coffee is specifically related with reduced brain AD pathologies in human. Hence, this study aims to investigate relationships between coffee intake and in vivo AD pathologies, including cerebral beta-amyloid (Aβ) deposition, the neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMH). A total of 411 non-demented older adults were included. Participants underwent comprehensive clinical assessment and multimodal neuroimaging including [11C] Pittsburgh compound B-positron emission tomography (PET), [18F] fluorodeoxyglucose PET, and magnetic resonance imaging scans. Lifetime and current coffee intake were categorized as follows: no coffee or <2 cups/day (reference category) and ≥2 cups/day (higher coffee intake). Lifetime coffee intake of ≥2 cups/day was significantly associated with a lower Aβ positivity compared to coffee intake of <2 cups/day, even after controlling for potential confounders. In contrast, neither lifetime nor current coffee intake was not related to hypometabolism, atrophy of AD-signature region, and WMH volume. The findings suggest that higher lifetime coffee intake may contribute to lowering the risk of AD or related cognitive decline by reducing pathological cerebral amyloid deposition.

2021 ◽  
Author(s):  
Jee Wook Kim ◽  
Min Soo Byun ◽  
Jun Ho Lee ◽  
Dahyun Yi ◽  
Min Jung Kim ◽  
...  

Abstract Background: Partner bereavement is one of life’s greatest stresses and has been suggested to trigger or accelerate cognitive decline and dementia. However, little information is available about potential brain pathologies underlying the association between partner bereavement and cognitive decline. Aims: We aimed to test the hypothesis that lifetime partner bereavement is associated with in vivo human brain pathologies underlying cognitive decline. Method: A total of 319 ever-married older adults between 61 and 90 years of age underwent comprehensive clinical assessments and multimodal brain imaging including [11C] Pittsburgh compound B-positron emission tomography (PET), AV-1451 PET, [18F] fluorodeoxyglucose (FDG)-PET, and magnetic resonance imaging. Results: Participants were classified as experiencing no partner bereavement or partner bereavement, and comparisons using propensity score matching (59 cases and 59 controls) were performed. Partner bereavement was significantly associated with higher cerebral white matter hyperintensities (WMH) volume compared to no partner bereavement. Interactions and subsequent subgroup analyses showed that partner bereavement was significantly associated with higher WMH in the older (>75 years) subgroup and among those with no- or low-skill occupations. In addition, partner bereavement at 60 years or over affect WMH volume compared to no partner bereavement, whereas partner bereavement at 60 years did not. No group differences were observed in other brain pathologies between partner bereavement categories. Conclusions: The findings suggest that the partner bereavement may contribute to dementia or cognitive decline by increasing cerebrovascular injury, particularly in older individuals and those with no- or low-skill occupations.


2019 ◽  
Vol 19 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Timo Grimmer ◽  
Oliver Goldhardt ◽  
Igor Yakushev ◽  
Marion Ortner ◽  
Christian Sorg ◽  
...  

Background: Neprilysin (NEP) cleaves amyloid-β 1–42 (Aβ42) in the brain. Hence, we aimed to elucidate the effect of NEP on Aβ42 in cerebrospinal fluid (CSF) and on in vivo brain amyloid load using amyloid positron emission tomography (PET) with [11C]PiB (Pittsburgh compound B). In addition, associations with the biomarkers for neuronal injury, CSF-tau and FDG-PET, were investigated. Methods: Associations were calculated using global and voxel-based (SPM8) linear regression analyses in the same cohort of 23 highly characterized Alzheimer’s disease patients. Results: CSF-NEP was significantly inversely associated with CSF-Aβ42 and positively with the extent of neuronal injury as measured by CSF-tau and FDG-PET. Conclusions: Our results on CSF-NEP are compatible with the assumption that local degradation, amongst other mechanisms of amyloid clearance, plays a role in the development of Alzheimer’s pathology. In addition, CSF-NEP is associated with the extent and the rate of neurodegeneration.


2020 ◽  
Vol 117 (49) ◽  
pp. 30928-30933
Author(s):  
Hong-Jun Cho ◽  
Truc T. Huynh ◽  
Buck E. Rogers ◽  
Liviu M. Mirica

Herein, we report a64Cu positron emission tomography (PET) imaging agent that shows appreciable in vivo brain uptake and exhibits high specific affinity for beta-amyloid (Aβ) aggregates, leading to the successful PET imaging of amyloid plaques in the brains of 5xFAD mice versus those of wild-type mice. The employed approach uses a bifunctional chelator with two Aβ-interacting fragments that dramatically improves the Aβ-binding affinity and lipophilicity for favorable blood–brain barrier penetration, while the use of optimized-length spacers between the Cu-chelating group and the Aβ-interacting fragments further improves the in vivo Aβ-binding specificity and brain uptake of the corresponding64Cu PET imaging agent.


2017 ◽  
Vol 37 (05) ◽  
pp. 538-545 ◽  
Author(s):  
Eduardo Caverzasi ◽  
Christian Cordano ◽  
Stephen Hauser ◽  
Roland Henry ◽  
Antje Bischof

Neuroimaging has emerged as a powerful technology that has enabled visualization of the impact of multiple sclerosis (MS) on the central nervous system in vivo with unprecedented precision. It has played a crucial role in disentangling the chronology of inflammation and neurodegeneration, developing and understanding mechanisms of novel therapeutics, and diagnosing and monitoring the disease in the clinical setting. However, challenges pertaining to the limited resolution, lack of specificity, inherent technological biases, and processing of increasingly big datasets have hindered comprehensive insights into the pathology underlying disability.Here, we review the advances in neuroimaging for MS that have moved the field forward in recent years by addressing the above-mentioned issues, thereby enhancing our knowledge of this yet enigmatic disease. We discuss complementary imaging technologies, including magnetic resonance imaging, positron emission tomography, and optical coherence tomography, the most recent tool in the MS imaging armamentarium that holds promise to act as a surrogate of pathological changes in the central nervous system in a more easily accessible way.


2010 ◽  
Vol 5 (6) ◽  
pp. 434-439 ◽  
Author(s):  
Fergus N. Doubal ◽  
Rosemarie de Haan ◽  
Thomas J. MacGillivray ◽  
Petra E. Cohn-Hokke ◽  
Bal Dhillon ◽  
...  

2008 ◽  
Vol 105 (10) ◽  
pp. 3705-3710 ◽  
Author(s):  
C. Catana ◽  
D. Procissi ◽  
Y. Wu ◽  
M. S. Judenhofer ◽  
J. Qi ◽  
...  

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