A review of Î²-amyloid neuroimaging in Alzheimer's disease

Adlard, Paul A.; Tran, Bob Anh; Finkelstein, David I.; Desmond, Patricia; Johnston, Leigh A.; Bush, Ashley I.; Egan, Gary F.

doi:10.3389/fnins.2014.00327

Cited by 86 publications

(63 citation statements)

References 183 publications

(454 reference statements)

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“…Although there is no absolute certainty, the accumulation of amyloid b (Ab) into senile plaques in the brain is hypothesized as a leading cause of AD, as these plaques have been found to cause progressive neuronal death [2,3]. Multiple pathogenic processes, including oxidative stress, inflammatory responses, and apoptosis, are implicated in Ab-induced neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Magnesium Lithospermate B Protects Neurons Against Amyloid β (1–42)-Induced Neurotoxicity Through the NF-κB Pathway

et al. 2015

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Magnesium lithospermate B (MLB) is one of the major bioactive components of Radix Salviae miltiorrhizae, a Chinese traditional herbal medicine colloquially known as Dan Shen. In this study, we investigated the neuroprotective effect of MLB against oligomeric amyloid β (Aβ) (1-42)-induced neurotoxicity in cultured FVB mouse hippocampal neurons. We found that pretreatment with MLB not only prevents a loss in neuronal cell viability following exposure to Aβ (1-42), but also attenuates Aβ (1-42)-induced release of pro-inflammatory cytokines and neuronal apoptosis in a dose-dependent manner. Mechanistic studies show that MLB counteracts Aβ (1-42)-induced activation of the nuclear factor kappa B (NF-κB) pathway, evidenced by the suppression of NF-κB luciferase reporters, decreased expression of phosphorylated Inhibitor κB α and IκB kinase α, and reduced nuclear translocation of p65 in response to pre-treatment with 50 μg/ml MLB prior to Aβ (1-42) exposure. MLB was able to reverse the increase in phosphorylated c-Jun N-terminal kinase (JNK) levels as well as the decrease in phosphorylated Akt levels that are induced by Aβ (1-42), although this finding did not extend to extracellular signal-regulated kinase or p38 kinases. Furthermore, combining MLB with the JNK inhibitor SP600125 synergistically counteracts the Aβ (1-42)-induced reduction in cell viability and neurite growth, and the neuroprotective effects of MLB could be attenuated by the Akt inhibitor triciribine. In conclusion, these results suggest that MLB can protect against Aβ (1-42)-induced neuronal damage, which is most likely to be mediated by the NK-κB pathway.

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Section: Introductionmentioning

confidence: 99%

Magnesium Lithospermate B Protects Neurons Against Amyloid β (1–42)-Induced Neurotoxicity Through the NF-κB Pathway

et al. 2015

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“…It also provides unique detection of AD pathology in the hippocampus [15,16]. However, the ability to bind amyloid plaque, neurofibrillary tangles, Lewy bodies, and prions may hinder the utility of FDNNP for routine imaging to distinguish AD from AD mimics [17][18][19][20]. This lack of discrimination along with poor signal-to-noise ratio is the rationale for the limited scope of this agent [21].…”

Section: Compounds Of Interestmentioning

confidence: 99%

Amyloid Imaging: Poised for Integration into Medical Practice

Anand

Sabbagh

2017

Neurotherapeutics

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Amyloid imaging represents a significant advance as an adjunct in the diagnosis of Alzheimer's disease (AD) because it is the first imaging modality that identifies in vivo changes known to be associated with the pathogenesis. Initially, 11 C-PIB was developed, which was the prototype for many 18 F compounds, including florbetapir, florbetaben, and flutemetamol, among others. Despite the high sensitivity and specificity of amyloid imaging, it is not commonly used in clinical practice, mainly because it is not reimbursed under current Center for Medicare and Medicaid Services guidelines in the USA. To guide the field in who would be most appropriate for the utility of amyloid positron emission tomography, current studies are underway [Imaging Dementia Evidence for Amyloid Scanning (IDEAS) Study] that will inform the field on the utilization of amyloid positron emission tomography in clinical practice. With the advent of monoclonal antibodies that specifically target amyloid antibody, there is an interest, possibly a mandate, to screen potential treatment recipients to ensure that they are suitable for treatment. In this review, we summarize progress in the field to date.

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“…Alzheimer's disease is the most common cause of dementia and is characterized by cognitive impairment, progressive neurodegeneration and formation of Ab-amyloid containing plaques and neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau [80]. One of the most significant developments in AD research has been the development to image the amyloid plaques, whose deposition and accumulation are viewed as fundamental to the pathological process leading to AD [81]. [ 11 C]PiB PET has been shown to be able to image Ab-amyloid plaques in the cortex many years before the clinical onset of the disease in patients with autosomal dominant AD [82], and has shown higher levels of Abamyloid deposits in early onset AD compared to late onset AD [83].…”

Section: Dementiamentioning

confidence: 99%

Recent imaging advances in neurology

2015

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Over the recent years, the application of neuroimaging techniques such as magnetic resonance imaging (MRI) and positron emission tomography (PET) has considerably advanced the understanding of complex neurological disorders. PET is a powerful molecular imaging tool, which investigates the distribution and binding of radiochemicals attached to biologically relevant molecules; as such, this technique is able to give information on biochemistry and metabolism of the brain in health and disease. MRI uses high intensity magnetic fields and radiofrequency pulses to provide structural and functional information on tissues and organs in intact or diseased individuals, including the evaluation of white matter integrity, grey matter thickness and brain perfusion. The aim of this article is to review the most recent advances in neuroimaging research in common neurological disorders such as movement disorders, dementia, epilepsy, traumatic brain injury and multiple sclerosis, and to evaluate their contribution in the diagnosis and management of patients.

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A review of Î²-amyloid neuroimaging in Alzheimer's disease

Cited by 86 publications

References 183 publications

Magnesium Lithospermate B Protects Neurons Against Amyloid β (1–42)-Induced Neurotoxicity Through the NF-κB Pathway

Magnesium Lithospermate B Protects Neurons Against Amyloid β (1–42)-Induced Neurotoxicity Through the NF-κB Pathway

Amyloid Imaging: Poised for Integration into Medical Practice

Recent imaging advances in neurology

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