Coffee intake and decreased amyloid pathology in human brain

Kim, Jee Wook; Byun, Min Soo; Yi, Dahyun; Lee, Jun Ho; Jeon, So Yeon; Jung, Gijung; Lee, Han Na; Sohn, Bo Kyung; Lee, Jun-Young; Kim, Yu Kyeong; Shin, Seong A.; Sohn, Chul‐Ho; Lee, Dong Hoon

doi:10.1038/s41398-019-0604-5

Cited by 67 publications

(69 citation statements)

References 49 publications

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“…One study investigated the relationships between coffee intake and in vivo AD pathologies, including cerebral Aβ deposition, the neurodegeneration of AD signature regions, and cerebral white matter hyper intensities. The results showed that lifetime coffee intake of ≥2 cups/day was significantly associated with a lower Aβ positivity compared to coffee intake of <2 cups/day, suggesting that higher lifetime coffee intake may contribute to lowering the risk of AD or related cognitive decline by reducing pathological cerebral amyloid deposition [119]. Similar results were achieved by Eskelinen et al [120].…”

Section: Rats Caffeic Acidsupporting

confidence: 78%

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

2019

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The positive role of nutrition in chronic neurodegenerative diseases (NDs) suggests that dietary interventions represent helpful tools for preventing NDs. In particular, diets enriched with natural compounds have become an increasingly attractive, non-invasive, and inexpensive option to support a healthy brain and to potentially treat NDs. Bioactive compounds found in vegetables or microalgae possess special properties able to counteract oxidative stress, which is involved as a triggering factor in neurodegeneration. Here, we briefly review the relevant experimental data on curcuminoids, silymarin, chlorogenic acid, and compounds derived from the microalga Aphanizomenon flos aquae (AFA) which have been demonstrated to possess encouraging beneficial effects on neurodegeneration, in particular on Alzheimer's disease models. and intracellular neurofibrillary tangles (NFTs) [4,5]. Intracellular neurofibrillary tangles are composed of hyperphosphorylated Tau proteins in neurons located particularly in the hippocampus and cerebral cortex regions of the brain. The reduced expression of the brain-derived neurotrophic factor (BDNF), important for neuronal growth and memory functions, also plays a crucial role in AD pathogenesis via formation of senile plaque of Aβ and NFTs. At the molecular level, Aβ induces oxidative stress, inflammation, and mitochondrial dysfunction associated with apoptosis [6,7].Parkinson's disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and formation of Lewy bodies, abnormal intraneuronal aggregates of proteins that include α-synuclein, ubiquitin, and neurofilaments [8]. The pathogenic mechanisms of PD include oxidative stress, mitochondrial and protein dysfunction, inflammation, and apoptosis [9]. In particular, oxidative stress generates ROS which activates glial cells, and activated glial cells generate inflammation that results in mitochondrial dysfunction, and, consequently, dysfunctional mitochondria activate cell death machinery [10].Hence, oxidative stress and mitochondrial damage are common factors involved in the etiopathology of these neurodegenerative diseases [11-13]. Oxidative Stress and NeurodegenerationOxidative stress is characterized by an overproduction of ROS-oxygen-containing molecules known to be highly reactive.Reactive oxygen species are formed in mitochondria during oxidative phosphorylation as a byproduct of normal metabolism. Therefore, modest levels of ROS are normally expected and are considered essential for the regulation of normal cell functions, while excessive ROS production can damage various biological targets, such as DNA, lipids, and proteins, causing serious neurological injury. Because the brain consumes a large amount of molecular oxygen to function properly, the accumulation of damaged biomolecules caused by ROS is high, especially with aging [14]. To limit these cellular damages, brain neurons produce antioxidant defense enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GPX) and catala...

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Section: Rats Caffeic Acidsupporting

confidence: 78%

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

2019

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“…This indicates that adequate adenosinergic activation is needed for normal memory function and that an over-or underactivation can lead to memory impairment [39]. This further explains why a recent study states coffee intake of ≥2 cups/day was significantly associated with a lower Aβ positivity compared to lower coffee drinkers (<2 cups/day), resulting in decreased cerebral amyloid deposition [40]. As the benefits of coffee on these disorders are much attributed to methylxanthines (i.e., caffeine), Figure 1 illustrates how inhibiting the subtypes of adenosine receptors can have different effects on them.…”

Section: Review Bioactive Compounds Of Coffee and Their Propertiesmentioning

confidence: 99%

Neuroprotective and Neurodegenerative Aspects of Coffee and Its Active Ingredients in View of Scientific Literature

Wasim

Kukkar

Awad

et al. 2020

Cureus

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Coffee and its components have several neuroprotective properties that lower the risk of cognitive decline and other neurodegenerative diseases. This study reviews the mechanisms by which coffee and its respective compounds affect the brain and its pathologies. Many epidemiological studies in this literature review have shown coffee to reduce the risk of developing dementia, stroke, and Alzheimer's disease. It may also have a positive impact on the disease course of amyotrophic lateral sclerosis, Parkinson's disease, and depression. The optimal benefits achieved from coffee in these pathologies rely on higher daily doses. Most of its effects are attributed to caffeine by the antagonism of adenosine receptors in the central nervous system; however, other coffee constituents like chlorogenic acids have also shown much promise in therapeutic value. Existing research considers coffee to have great potential, but additional studies are still needed to clarify the mechanisms and actual causal relationships in certain neuropathologies.

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“…However, a 2018 dose-response meta-analysis of 8 prospective studies found no significant association between caffeine dosage and risk of AD or dementia [371]. Nevertheless, a 2019 study found that compared to drinking less than two cups of coffee a day, lifetime drinking two or more cups of coffee a day was significantly associated with reduced A␤ plaque burden in 411 cognitively-intact older adults [372]. Therefore, caffeine intake may be associated with a decreased risk of dementia, cognitive decline, and/or AD.…”

Section: Caffeinementioning

confidence: 99%

“…No clinical trials performed. May decrease risk of dementia, cognitive decline, and AD [213,364,[367][368][369][370][371][372]. Propentofylline Broad-spectrum PDE inhibitor [340] May be effective and indicated for the treatment of vascular dementia and AD [375,376,[387][388][389][390][391].…”

Section: Propentofyllinementioning

confidence: 99%

Phosphodiesterase Inhibitors for Alzheimer’s Disease: A Systematic Review of Clinical Trials and Epidemiology with a Mechanistic Rationale

Sanders

Rajagopal²

2020

ADR

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Background: Preclinical studies, clinical trials, and reviews suggest increasing 3',5'-cyclic adenosine monophosphate (cAMP) and 3',5'-cyclic guanosine monophosphate (cGMP) with phosphodiesterase inhibitors is disease-modifying in Alzheimer's disease (AD). cAMP/protein kinase A (PKA) and cGMP/protein kinase G (PKG) signaling are disrupted in AD. cAMP/PKA and cGMP/PKG activate cAMP response element binding protein (CREB). CREB binds mitochondrial and nuclear DNA, inducing synaptogenesis, memory, and neuronal survival gene (e.g., brain-derived neurotrophic factor) and peroxisome proliferator-activated receptor-␥ coactivator-1␣ (PGC1␣). cAMP/PKA and cGMP/PKG activate Sirtuin-1, which activates PGC1␣. PGC1␣ induces mitochondrial biogenesis and antioxidant genes (e.g.,Nrf2) and represses BACE1. cAMP and cGMP inhibit BACE1-inducing NFκB and tau-phosphorylating GSK3␤. Objective and Methods: We review efficacy-testing clinical trials, epidemiology, and meta-analyses to critically investigate whether phosphodiesteraseinhibitors prevent or treat AD. Results: Caffeine and cilostazol may lower AD risk. Denbufylline and sildenafil clinical trials are promising but preliminary and inconclusive. PF-04447943 and BI 409,306 are ineffective. Vinpocetine, cilostazol, and nicergoline trials are mixed. Deprenyl/selegiline trials show only short-term benefits. Broad-spectrum phosphodiesterase inhibitor propentofylline has been shown in five phase III trials to improve cognition, dementia severity, activities of daily living, and global assessment in mild-to-moderate AD patients on multiple scales, including the ADAS-Cogand the CIBIC-Plus in an 18-month phase III clinical trial. However, two books claimed based on a MedScape article an 18-month phase III trial failed, so propentofylline was discontinued. Now, propentofylline is used to treat canine cognitive dysfunction, which, like AD, involves age-associated wild-type A␤ deposition. Conclusion: Phosphodiesterase inhibitors may prevent and treat AD.

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Coffee intake and decreased amyloid pathology in human brain

Cited by 67 publications

References 49 publications

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

Neuroprotective and Neurodegenerative Aspects of Coffee and Its Active Ingredients in View of Scientific Literature

Phosphodiesterase Inhibitors for Alzheimer’s Disease: A Systematic Review of Clinical Trials and Epidemiology with a Mechanistic Rationale

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