scholarly journals Alzheimer's disease: the amyloid hypothesis and the Inverse Warburg effect

2015 ◽  
Vol 5 ◽  
Author(s):  
Lloyd A. Demetrius ◽  
Pierre J. Magistretti ◽  
Luc Pellerin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Warburg Effect ◽  
Amyloid Hypothesis

Neuroinflammation and Alzheimer’s disease: lessons learned from 5-lipoxygenase

2014 ◽  
Vol 5 (3) ◽  
Author(s):  
Yash Joshi ◽  
Domenico Praticò
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Amyloid Beta ◽  
Neuronal Cells ◽  
Lessons Learned ◽  
Brain Inflammation ◽  
Complex Relationship ◽  
Amyloid Hypothesis

AbstractAside from the well-known amyloid beta and tau pathologies found in Alzheimer’s disease (AD), neuroinflammation is a well-established aspect described in humans and animal models of the disease. Inflammatory perturbations are evident not only in neurons, but also in non-neuronal cells and cytokines in the AD brain. Although the amyloid hypothesis implicates amyloid beta (Aβ) as the prime initiator of the AD, brain inflammation in AD has a complex relationship between Aβ and tau. Using our work with the 5-lipoxygenase protein as an example, we suggest that at least in the case of AD, there is an interdependent and not necessarily hierarchical pathological relationship between Aβ, tau and inflammation.

O4-05-05: Modeling familial danish dementia: Implications for the amyloid hypothesis of Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. S158-S158
Author(s):  
Janaky Coomaraswamy ◽  
Ellen Kilger ◽  
Heidrun Woelfing ◽  
Claudia Schaefer ◽  
Stephan A. Kaeser ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Hypothesis ◽  
Familial Danish Dementia

scholarly journals Alzheimer's disease: The amyloid hypothesis on trial

2016 ◽  
Vol 208 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Judith R. Harrison ◽  
Michael J. Owen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Drug Trials ◽  
Amyloid Hypothesis ◽  
Directed Research

SummaryThe pathogenesis of Alzheimer's disease is complex. The amyloid hypothesis has directed research efforts for many years, but it has recently been questioned after failed drug trials. Here, we review the evidence for and against and suggest that it might be premature to abandon the amyloid hypothesis.

scholarly journals he amyloid hypothesis of Alzheimer's disease: past and present, hopes and disappointments

2019 ◽  
Vol 11 (3) ◽  
pp. 4-10
Author(s):  
I. V. Litvinenko ◽  
A. Yu. Emelin ◽  
V. Yu. Lobzin ◽  
K. A. Kolmakova ◽  
K. M. Naumov ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Signs ◽  
Passive Immunization ◽  
Amyloid Hypothesis ◽  
Amyloid Deposits ◽  
Redox Active ◽  
Protein Overproduction ◽  
The Brain

In 1887, S.A. Belyakov, a physician of the Imperial Medical and Surgical Academy, first described amyloid deposits in the brain of patients with dementia. Later, in 1906, A. Alzheimer revealed amyloid plaques and tau tangles in a patient with clinical signs of dementia. Over the following 100 years, the development of the concept of the amyloid origin of Alzheimer's disease (AD) confirmed numerous relationships between the brain accumulation of APs and cognitive decline. And if at the beginning of the amyloid era many researchers considered that the disease was caused by amyloid beta (Aβ) protein overproduction, in recent years they have increasingly pointed to a defect in the mechanisms of Aβ clearance, especially after the discovery of the lymphatic system of the brain. The role of disturbed homeostasis of redox-active metals, primarily iron and copper, in the development of the disease is also considered.The amyloid hypothesis of AD has served as the basis for several areas in the design of drugs, such as secretase inhibitors, immunomodulatory drugs for active and passive immunization. However, only one drug (Akatinol memantine, an inhibitor of NMDA receptors and glutamatergic excitotoxicity) for the treatment of AD has been introduced into clinical practice over the past 20 years. Of interest are the data obtained in new studies of Akatinol memantine, which suggest that the latter is able to some extent affect the main pathophysiological processes underlying the development of cognitive impairment in Alzheimer-type pathology. 

scholarly journals Exploring the Potential of Therapeutic Agents Targeted towards Mitigating the Events Associated with Amyloid-β Cascade in Alzheimer’s Disease

2020 ◽  
Vol 21 (20) ◽  
pp. 7443 ◽  
Author(s):  
Tapan Behl ◽  
Ishnoor Kaur ◽  
Ovidiu Fratila ◽  
Roxana Brata ◽  
Simona Bungau
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Therapeutic Agents ◽  
Active Immunotherapy ◽  
Amyloid Hypothesis ◽  
Neuronal Connections ◽  
Glucagon Like Peptide 1 ◽  
Natural Drugs ◽  
Enzymatic Pathways

One of the most commonly occurring neurodegenerative disorders, Alzheimer’s disease (AD), encompasses the loss of cognitive and memory potential, impaired learning, dementia and behavioral defects, and has been prevalent since the 1900s. The accelerating occurrence of AD is expected to reach 65.7 million by 2030. The disease results in neural atrophy and disrupted inter-neuronal connections. Amongst multiple AD pathogenesis hypotheses, the amyloid beta (Aβ) cascade is the most relevant and accepted form of the hypothesis, which suggests that Aβ monomers are formed as a result of the cleavage of amyloid precursor protein (APP), followed by the conversion of these monomers to toxic oligomers, which in turn develop β-sheets, fibrils and plaques. The review targets the events in the amyloid hypothesis and elaborates suitable therapeutic agents that function by hindering the steps of plaque formation and lowering Aβ levels in the brain. The authors discuss treatment possibilities, including the inhibition of β- and γ-secretase-mediated enzymatic cleavage of APP, the immune response generating active immunotherapy and passive immunotherapeutic approaches targeting monoclonal antibodies towards Aβ aggregates, the removal of amyloid aggregates by the activation of enzymatic pathways or the regulation of Aβ circulation, glucagon-like peptide-1 (GLP-1)-mediated curbed accumulation and the neurotoxic potential of Aβ aggregates, bapineuzumab-mediated vascular permeability alterations, statin-mediated Aβ peptide degradation, the potential role of ibuprofen and the significance of natural drugs and dyes in hindering the amyloid cascade events. Thus, the authors aim to highlight the treatment perspective, targeting the amyloid hypothesis, while simultaneously emphasizing the need to conduct further investigations, in order to provide an opportunity to neurologists to develop novel and reliable treatment therapies for the retardation of AD progression.

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