Molecular mechanisms linking amyloid β toxicity and Tau hyperphosphorylation in Alzheimer׳s disease

Lloret, Ana; Fuchsberger, Tanja; Giraldo, Esther; Viña, José

doi:10.1016/j.freeradbiomed.2015.02.028

Cited by 112 publications

(98 citation statements)

References 89 publications

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“…Similar mechanism with microglia activation along with existing cellular stress and chronic inflammation has significant role in the pathophysiology of neurodegenerative diseases [8,114]. In AD and ALS patients, abnormal phosphorylation of proteins has been observed and intriguingly, IL-1 positive microglia also found in such pathologies, which confers the putative role of inflammatory mediators in neurodegenerative pathology [116,117]. Moreover, it's been always consistent that, neuroinflammation accompanied with oxidative stress exerts detrimental consequence in chronic neurodegenerative disease profile.…”

Section: Neuroinflammation and Neurodegeneration: A Tale Of Promise Amentioning

confidence: 79%

“…Moreover, Th17 also capable of influencing the secretion of IL-17, which in turn assists increased secretion of other detrimental inflammatory factors like tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) [122][123][124]. In this way Th17 spreads the inflammatory responses promptly throughout the brain by activating microglial population [116]. On the other hand, expression of MDSCs is known to inhibit inflammation, which is quite opposite to the function of Th17 [125][126][127].…”

Section: Review Effect and Disease Indicative Role Of Inflammation Inmentioning

confidence: 99%

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Effect and Disease Indicative Role of Inflammation in Neurodegenerative Pathology: A Mechanistic Crosstalk of Promise and Dilemma

Choudhury¹,

Chakraborty²,

Banerjee³

et al. 2018

Neuropsychiatry

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The pathobiology of neuronal cell loss due to various endogenous or exogenous influences is clinically termed as neurodegeneration. Neurodegeneration has been reported to be the major contributor to aging and central nervous system diseases. Apart from aging and endogenous involvement, neurodegeneration also has been reported from viral infection and prion diseases. Studies have shown that, chronic degeneration of neuronal cells initiate the pathology of Alzheimer's disease-the most prevalent neurodegenerative disorder in the world. Similar neurodegenerative pathology is also evident in Parkinson's disease, multiple sclerosis, and Amyotrophic Lateral Sclerosis. Neurodegeneration negatively affects the mental and physical functioning of the patient. Intriguingly, the involvement of inflammation has been linked as the most crucial entity in the mechanistic progress of neurodegeneration. Moreover, recent data also have shown that inflammatory biomarkers can prognosticate the silent progress of neurodegeneration through low-cost diagnostic approach. Mainly, Th17 and MDSCs are the particular immune cells, which have been reported to assist adequately to get a detailed insight into the underlying pathological process in neurodegeneration. Similarly, depression and dementia are also having a crucial association with pro-inflammatory cytokines, which in chronic spectrum indicates the degenerative pathology. Together, available literatures are depicting a direct association between neuroinflammation and neurodegeneration. In the present review, we have summed up all the neuropathologies in light of inflammation and emphasized the possible diagnostic measures by using inflammatory cells and mediators as biomarkers for neurodegenerative diseases.

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Section: Neuroinflammation and Neurodegeneration: A Tale Of Promise Amentioning

confidence: 79%

Section: Review Effect and Disease Indicative Role Of Inflammation Inmentioning

confidence: 99%

Effect and Disease Indicative Role of Inflammation in Neurodegenerative Pathology: A Mechanistic Crosstalk of Promise and Dilemma

Choudhury¹,

Chakraborty²,

Banerjee³

et al. 2018

Neuropsychiatry

View full text Add to dashboard Cite

show abstract

“…The Aβ extracellular plaques are present in the brain parenchyma, being essentially composed of Aβ peptides in which the N-terminus is truncated. Several studies show that Aβ deposition occurs early in AD onset (up to 20 years prior to symptom manifestation), being able to induce tau phosphorylation inside neuronal cells and NFT formation (reviewed by Lloret et al [27]).…”

Section: Ad and Its Hallmarksmentioning

confidence: 99%

Glia-Mediated Retinal Neuroinflammation as a Biomarker in Alzheimer's Disease

Madeira

Ambrósio²,

Santiago³

2015

Ophthalmic Res

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Alzheimer's disease (AD) is the most common type of dementia worldwide; it is characterized by a progressive decline in cognitive functions and memory, resulting from synaptic and cell loss, and accompanied by a strong neuroinflammatory response. Besides the vast progress in the understanding of the pathophysiology of AD in the past decades, there is still no effective treatment. Moreover, the diagnosis occurs usually at an advanced stage of the disease, where the neurological damage has already occurred. The identification of biomarkers that would allow an early diagnosis of this disease is a major goal that would also help managing AD progression. Due to its cellular and physiological resemblances with the brain, the retina has long been regarded as a window to the brain. Several brain manifestations have been associated with retinal alterations. In AD patients, some structural and functional alterations in the retina can be associated with disease onset. However, only a few studies have focused on the alterations in retinal glial cells associated with AD. This review aims at giving an overview of the AD-associated retinal alterations, particularly in glial cells. The documented alterations in retinal glia will be discussed concerning their potential to predict the brain alterations occurring in AD.

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“…Although controversy remains regarding which of the two may be the primary culprit, recent evidence suggests that expression of these two markers may be linked. 3 The problem with targeting either or both as a therapy is that in both cases APP (from which amyloid is abnormally cleaved) and tau protein are virtually ubiquitous features of all neurons; hence, we need to identify a constraining additional feature that would explain why only certain neurons are vulnerable. 4 Drugs that combat either amyloid or hyperphosphorylated tau may have some benefit, but they would not intervene at the basic mechanism.…”

Section: Why So Many Drugs Have Failedmentioning

confidence: 99%