ReviewFrontiers in aging neuroscience2014
Alzheimer's disease: relevant molecular and physiopathological events affecting amyloid-β brain balance and the putative role of PPARs.
Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Chronic inhibition of receptor protein tyrosine phosphatase β/ζ reduces amyloid plaque load and modulates pleiotrophin-expressing glial cells, glial-plaque interactions and genes related to amyloid beta clearance.Frontiers in pharmacology · 2026Article
- Liver dysfunction triggers early Alzheimer's pathology in an adult rat model of chronic liver disease.Scientific reports · 2025Article
- Lipidopathy disrupts peripheral and central amyloid clearance in Alzheimer's disease: Where are our knowledge.IBRO neuroscience reports · 2025Review
- Effects silymarin and rosuvastatin on amyloid-carriers level in dyslipidemic Alzheimer's patients: A double-blind placebo-controlled randomized clinical trial.IBRO neuroscience reports · 2024Article
- Advances in Blood Biomarkers for Alzheimer's Disease: Ultra-Sensitive Detection Technologies and Impact on Clinical Diagnosis.Degenerative neurological and neuromuscular disease · 2024Review
- Ginsenoside Rg1 alleviates learning and memory impairments and Aβ disposition through inhibiting NLRP1 inflammasome and autophagy dysfunction in APP/PS1 mice.Molecular medicine reports · 2023Article
- The Neurovascular Unit Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Low Liver Enzymes and Risk of Dementia: The Atherosclerosis Risk in Communities (ARIC) Study.Journal of Alzheimer's disease : JAD · 2021Article
- β-Secretase1 biological markers for Alzheimer's disease: state-of-art of validation and qualification.Alzheimer's research & therapy · 2020Review
- Is Alzheimer's Disease a Liver Disease of the Brain?Journal of Alzheimer's disease : JAD · 2020Review
- Peroxisome turnover and diurnal modulation of antioxidant activity in retinal pigment epithelia utilizes microtubule-associated protein 1 light chain 3B (LC3B).American journal of physiology. Cell physiology · 2019Article
- Treadmill Exercise Ameliorates Spatial Learning and Memory Deficits Through Improving the Clearance of Peripheral and Central Amyloid-Beta Levels.Neurochemical research · 2018Article
- PPARs and Energy Metabolism Adaptation during Neurogenesis and Neuronal Maturation.International journal of molecular sciences · 2018Review
- Dendrobium nobile Lindl. Alkaloids Decreases the Level of Intracellular β-Amyloid by Improving Impaired Autolysosomal Proteolysis in APP/PS1 Mice.Frontiers in pharmacology · 2018Article
- 1, 25-DFrontiers in cellular neuroscience · 2018Article
- Impact of Rye Kernel-Based Evening Meal on Microbiota Composition of Young Healthy Lean Volunteers With an Emphasis on Their Hormonal and Appetite Regulations, and Blood Levels of Brain-Derived Neurotrophic Factor.Frontiers in nutrition · 2018Article
- Evidence to Consider Angiotensin II Receptor Blockers for the Treatment of Early Alzheimer's Disease.Cellular and molecular neurobiology · 2016Review
- Extra-virgin olive oil attenuates amyloid-β and tau pathologies in the brains of TgSwDI mice.The Journal of nutritional biochemistry · 2015Article
- Oleocanthal enhances amyloid-β clearance from the brains of TgSwDI mice and in vitro across a human blood-brain barrier model.ACS chemical neuroscience · 2015Article
- Mitochondrial dysfunction in diabetic neuropathy: a series of unfortunate metabolic events.Current diabetes reports · 2015Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common form of age-related dementia. With the expected aging of the human population, the estimated morbidity of AD suggests a critical upcoming health problem. Several lines of research are focused on understanding AD pathophysiology, and although the etiology of the disease remains a matter of intense debate, increased brain levels of amyloid-β (Aβ) appear to be a critical event in triggering a wide range of molecular alterations leading to AD. It has become evident in recent years that an altered balance between production and clearance is responsible for the accumulation of brain Aβ. Moreover, Aβ clearance is a complex event that involves more than neurons and microglia. The status of the blood-brain barrier (BBB) and choroid plexus, along with hepatic functionality, should be considered when Aβ balance is addressed. Furthermore, it has been proposed that exposure to sub-toxic concentrations of metals, such as copper, could both directly affect these secondary structures and act as a seeding or nucleation core that facilitates Aβ aggregation. Recently, we have addressed peroxisomal proliferator-activated receptors (PPARs)-related mechanisms, including the direct modulation of mitochondrial dynamics through the PPARγ-coactivator-1α (PGC-1α) axis and the crosstalk with critical aging- and neurodegenerative-related cellular pathways. In the present review, we revise the current knowledge regarding the molecular aspects of Aβ production and clearance and provide a physiological context that gives a more complete view of this issue. Additionally, we consider the different structures involved in AD-altered Aβ brain balance, which could be directly or indirectly affected by a nuclear receptor (NR)/PPAR-related mechanism.
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