Inactivation of GAP-43 due to the depletion of cellular calcium by the Pb and amyloid peptide induced toxicity: An in vitro approach

Ayyalasomayajula, Neelima; Bandaru, Madhuri; Dixit, Prasanna Kumar; Ajumeera, Rajanna; Chetty, C. S.; Challa, Suresh

doi:10.1016/j.cbi.2019.108927

Cited by 16 publications

(5 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[ [23][24][25][172][173][174] Manganese Manganese exposure increased the transcription of BACE1 in PC12 cells [27] Silver nanoparticles Silver nanoparticle exposure increased the protein expression of BACE1 [32] Zinc Zinc exposure increased BACE1 in mice and SH-SY5Y cells [175] Pesticides, fungicides, herbicides DDT DDT exposure increased BACE1 levels in SH-SY5Y cells [33] Paraquat Paraquat treatment altered BACE1 subcellular compartmentalization [36] Rotenone Rotenone treatment facilitated BACE1 expression and activity [34] Residues of cyprodinil, mepanipyrim, and pyrimethanil…”

Section: Metalsmentioning

confidence: 99%

Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target

Syeda

Cannon

2021

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Alzheimer's disease (AD) is a major public health crisis due to devastating cognitive symptoms, a lack of curative treatments, and increasing prevalence. Most cases are sporadic (>95% of cases) after the age of 65 years, implicating an important role of environmental factors in disease pathogenesis. Environmental neurotoxicants have been implicated in neurodegenerative disorders including Parkinson's Disease and AD. Animal models of AD and in vitro studies have shed light on potential neuropathological mechanisms, yet the biochemical and molecular underpinnings of AD‐relevant environmental neurotoxicity remain poorly understood. Beta‐site amyloid precursor protein cleaving enzyme 1 (BACE1) is a potentially critical pathogenic target of environmentally induced neurotoxicity. BACE1 clearly has a critical role in AD pathophysiology: It is required for amyloid beta production and expression and activity of BACE1 are increased in the AD brain. Though the literature on BACE1 in response to environmental insults is limited, current studies, along with extensive AD neurobiology literature suggest that BACE1 deserves attention as an important neurotoxic target. Here, we critically review research on environmental neurotoxicants such as metals, pesticides, herbicides, fungicides, polyfluoroalkyl substances, heterocyclic aromatic amines, advanced glycation end products, and acrolein that modulate BACE1 and potential mechanisms of action. Though more research is needed to clearly understand whether BACE1 is a critical mediator of AD‐relevant neurotoxicity, available reports provide convincing evidence that BACE1 is altered by environmental risk factors associated with AD pathology, implying that BACE1 inhibition and its use as a biomarker should be considered in AD management and research.

show abstract

Section: Metalsmentioning

confidence: 99%

Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target

Syeda

Cannon

2021

J Biochem & Molecular Tox

View full text Add to dashboard Cite

show abstract

“…When GAP-43 is phosphorylated, it encourages the growth of neurites and boosts vesicle cycling, which leads to heightened neuronal plasticity [ 72 ]. Furthermore, PSD-95 is a postsynaptic scaffolding protein that participates in the development and malleability of synapses [ 73 ]. Consistent with prior findings, treatment with Coriolus versicolor boosts the production of GAP-43, a presynaptic protein, and PSD-95, a postsynaptic protein, in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Action of Natural Compounds in Peripheral Multiorgan Dysfunction and Hippocampal Neuroinflammation Induced by Sepsis

et al. 2023

View full text Add to dashboard Cite

Bacterial sepsis induces the production of excessive pro-inflammatory cytokines and oxidative stress, resulting in tissue injury and hyperinflammation. Patients recovering from sepsis have increased rates of central nervous system (CNS) morbidities, which are linked to long-term cognitive impairment, such as neurodegenerative pathologies. This paper focuses on the tissue injury and hyperinflammation observed in the acute phase of sepsis and on the development of long-term neuroinflammation associated with septicemia. Here we evaluate the effects of Coriolus versicolor administration as a novel approach to treat polymicrobial sepsis. Rats underwent cecal ligation and perforation (CLP), and Coriolus versicolor (200 mg/kg in saline) was administered daily by gavage. Survival was monitored, and tissues from vital organs that easily succumb to infection were harvested after 72 h to evaluate the histological changes. Twenty-eight days after CLP, behavioral analyses were performed, and serum and brain (hippocampus) samples were harvested at four weeks from surgery. Coriolus versicolor increased survival and reduced acute tissue injury. Indeed, it reduced the release of pro-inflammatory cytokines in the bloodstream, leading to a reduced chronic inflammation. In the hippocampus, Coriolus versicolor administration restored tight junction expressions, reduce cytokines accumulation and glia activation. It also reduced toll-like receptor 4 (TLR4) and neuronal nitric oxide synthase (nNOS) and the NLR family pyrin domain containing 3 (NLRP3) inflammasome components expression. Coriolus versicolor showed antioxidant activities, restoring glutathione (GSH) levels and catalase and superoxide dismutase (SOD) activities and reducing lipid peroxidation, nitrite and reactive oxygen species (ROS) levels. Importantly, Coriolus versicolor reduced amyloid precursor protein (APP), phosphorylated-Tau (p-Tau), pathologically phosphorylated tau (PHF1), phosphorylated tau (Ser202 and Thr205) (AT8), interferon-induced transmembrane protein 3 (IFITM3) expression, and β-amyloid accumulation induced by CLP. Indeed, Coriolus versicolor restored synaptic dysfunction and behavioral alterations. This research shows the effects of Coriolus versicolor administration on the long-term development of neuroinflammation and brain dysfunction induced by sepsis. Overall, our results demonstrated that Coriolus versicolor administration was able to counteract the degenerative process triggered by sepsis.

show abstract

“…Growth-associated protein-43 (GAP-43) is a growth-related presynaptic protein that is highly expressed in the human hippocampus and is known to play an important role in the regulation of axonal growth, synaptic plasticity, learning, and memory. [ 30 ] Previous studies have found that GAP-43 is closely related to AD and is involved in the pathophysiology of AD. The Enzyme Linked Immunosorbent Assay technology was used to detect GAP-43 in human cerebrospinal fluid, and GAP-43 showed a high level of expression in the cerebrospinal fluid of AD patients, which was consistent with the changes of T-tau and P-tau.…”

Section: Biomarkers In Cerebrospinal Fluidmentioning

confidence: 99%

Research progress on humoral biomarkers of Alzheimer’s disease: A review

Zhang,

Fu,

Yang

et al. 2024

Medicine

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive memory loss. The main pathological features are neuronal fibrillary tangles caused by amyloid beta deposition and hyperphosphorylation of tau protein, accompanied by neuronal death and loss of synaptic structure. Early diagnosis is the key to the treatment of AD. It is known that some small molecular components are related to the pathogenesis of AD. This article will summarize the common AD biomarkers in cerebrospinal fluid and blood and analyze the current status of AD biomarkers and future research directions. This review summarizes the promising biomarkers for the diagnosis of AD in the last decade and describes their changes in AD body fluids. The diagnostic biomarkers related to AD were mainly distributed in cerebrospinal fluid and blood. Significant changes in these molecules can be detected in cerebrospinal fluid and blood, and they are correlated with AD severity. These humoral molecules have necessary relationship with AD and can be used as AD biomarkers to assist early diagnosis of AD.

show abstract

Inactivation of GAP-43 due to the depletion of cellular calcium by the Pb and amyloid peptide induced toxicity: An in vitro approach

Cited by 16 publications

References 39 publications

Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target

Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target

Mechanism of Action of Natural Compounds in Peripheral Multiorgan Dysfunction and Hippocampal Neuroinflammation Induced by Sepsis

Research progress on humoral biomarkers of Alzheimer’s disease: A review

Contact Info

Product

Resources

About