Moving Away from Amyloid Beta to Move on in Alzheimer Research

Moreno-Treviño, María Guadalupe; Castillo-López, Jesús; Meester, Irene

doi:10.3389/fnagi.2015.00002

Cited by 17 publications

(12 citation statements)

References 56 publications

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“…Moreover, the increase in the signal near 55 kDa was observed in AD cases in vulnerable cortical areas according to Braak's hierarchical scheme of NFT progression (TC) as well as in less affected areas (cerebellum). These observations support previous data indicating that in AD development of AP does not precede that of tau lesions nor is Aβ essential for tau progression [43,44,45,46,47,48]. As recently suggested in amyloid and tau imaging studies, Aβ formation may potentiate cellular neurodegeneration, but the two phenomena are largely independent in the human brain [for review see [49]].…”

Section: Discussionsupporting

confidence: 78%

A Study of Aβ Oligomers in the Temporal Cortex and Cerebellum of Patients with Neuropathologically Confirmed Alzheimer's Disease Compared to Aged Controls

et al. 2016

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Background/Aims: Investigations of Aβ oligomers in neuropathologically confirmed Alzheimer's disease (AD) are still scarce. We report neurohistopathological and biochemical analyses using antibodies against tau and amyloid β (Aβ) pathology. Methods: Thirty elderly AD patients and 43 age-matched controls with or without deposition of amyloid plaques (AP) were analyzed by immunohistochemistry. In 21 cases with available fresh tissue, Western blots were also performed. Neuropathological analysis included quantitative assessment of neurofibrillary tangles (NFT), AP and Aβ oligomer densities in the mesial temporal cortex (TC). Results: NFT, fibrillar amyloid and Aβ oligomeric deposit densities were significantly higher in AD patients than in controls. There was no relationship between oligomeric Aβ densities and Braak NFT staging scores. Furthermore, Aβ oligomer expression was closely correlated with Aβ plaques in the TC. By Western blot, Aβ oligomers were observed in AD patients, in plaque-free controls, in 1 ‘tangle-only AD' case, as well as in the cerebellum. A band near 55 kDa was the only Western blot signal that was significantly increased in the TC of AD patients compared to controls as well as less expressed in the cerebellum. Conclusion: These results suggest that a putative dodecamer, near 55 kDa, may contribute to AD vulnerability of the TC.

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Section: Discussionsupporting

confidence: 78%

A Study of Aβ Oligomers in the Temporal Cortex and Cerebellum of Patients with Neuropathologically Confirmed Alzheimer's Disease Compared to Aged Controls

et al. 2016

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“…Periodic reactivation of HHV-1 can be asymptomatic, unless the immune system is weakened, for example because of aging, stress, immunosuppression or peripheral infections [ 47 ]. In these circumstances, the virus is propagated freely, taking up several nerve cells, which involves a cascade of intracellular changes leading to cell death and neuro- degeneration of other areas of the brain [ 48 ]. HHV-1 acts directly, causing the cell machinery to produce viral proteins and indirectly via an inflammatory process.…”

Section: Infections and Admentioning

confidence: 99%

The Infectious Etiology of Alzheimer’s Disease

2017

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Background: Inflammation is a part of the first line of defense of the body against invasive pathogens, and plays a crucial role in tissue regeneration and repair. A proper inflammatory response ensures the suitable resolution of inflammation and elimination of harmful stimuli, but when the inflammatory reactions are inappropriate it can lead to damage of the surrounding normal cells. The relationship between infections and Alzheimer’s Disease (AD) etiology, especially late-onset AD (LOAD) has been continuously debated over the past three decades.Methods: This review discusses whether infections could be a causative factor that promotes the progression of AD and summarizes recent investigations associating infectious agents and chronic inflammation with AD. Preventive and therapeutic approaches to AD in the context of an infectious etiology of the disease are also discussed.Results: Emerging evidence supports the hypothesis of the role of neurotropic viruses from the Herpesviridae family, especially Human herpesvirus 1 (HHV-1), Cytomegalovirus (CMV), and Human herpesvirus 2 (HHV-2), in AD neuropathology. Recent investigations also indicate the association between Hepatitis C virus (HCV) infection and dementia. Among bacteria special attention is focused on spirochetes family and on periodontal pathogens such as Porphyromonas gingivalis or Treponema denticola that could cause chronic periodontitis and possibly contribute to the clinical onset of AD.Conclusion: Chronic viral, bacterial and fungal infections might be causative factors for the inflammatory pathway in AD.

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“…While the first is composed of amyloid-β (Aβ) peptides, the latter consists of hyper-phosphorylated tau-protein (reviewed in Bloom, 2014 ). The causal nature of Aβ-pathology is still under debate and findings of Aβ-accumulations without clinical manifestations question a strict relationship between Aβ-plaques formation and AD-symptoms for late-onset sporadic AD (reviewed in Moreno-Trevino et al, 2015 ). In contrast, mutations in the amyloid precursor protein (APP) as well as in presenilin 1 and 2 (PSEN1, 2) which participate in APP-processing cause hereditary early onset AD (Selkoe, 2001 ; Haass et al, 2012 ).…”

Section: Alzheimers Disease (Ad)mentioning

confidence: 99%

Chatting with the neighbors: crosstalk between Rho-kinase (ROCK) and other signaling pathways for treatment of neurological disorders

2015

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ROCK inhibition has been largely applied as a strategy to treat neurodegenerative diseases (NDDs) and promising results have been obtained in the recent years. However, the underlying molecular and cellular mechanisms are not fully understood and different models have been proposed for neurodegenerative disorders. Here, we aim to review the current knowledge obtained for NDDs identifying common mechanisms as well as disease-specific models. In addition to the role of ROCK in different cell types such as neurons and microglia, we focus on the molecular signaling-pathways which mediate the beneficial effects of ROCK. Besides canonical ROCK signaling, modulation of neighboring pathways by non-canonical ROCK-crosstalk is a recurrent pattern in many NDD-model systems and has been suggested to mediate beneficial effects of ROCK-inhibition.

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Moving Away from Amyloid Beta to Move on in Alzheimer Research

Cited by 17 publications

References 56 publications

A Study of Aβ Oligomers in the Temporal Cortex and Cerebellum of Patients with Neuropathologically Confirmed Alzheimer's Disease Compared to Aged Controls

A Study of Aβ Oligomers in the Temporal Cortex and Cerebellum of Patients with Neuropathologically Confirmed Alzheimer's Disease Compared to Aged Controls

The Infectious Etiology of Alzheimer’s Disease

Chatting with the neighbors: crosstalk between Rho-kinase (ROCK) and other signaling pathways for treatment of neurological disorders

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