Does the term ‘trophic’ actually mean anti-amyloidogenic? The case of NGF

Calissano, Pietro; Amadoro, Giuseppina; Matrone, Carmela; Ciafrè, Stefania; Marolda, Roberta; Corsetti, Veronica; Ciotti, Maria Teresa; Mercanti, Delio; Luzio, A. Di; Severini, Cinzia; Provenzano, Claudia; Canu, Nadia

doi:10.1038/cdd.2010.38

Cited by 31 publications

(32 citation statements)

References 90 publications

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“…This neurotrophin ensures the preservation of the biochemical and morphological phenotypes of the aforementioned neurons and their survival in the presence of damaging factors [4]. NGF inhibits the formation of amyloid plaques and neurofibrillary tangles in the brain – the main pathomorphological characteristics of AD – via the inhibition of amyloidogenic processing of APP [5] and hyperphosphorylation of the tau protein, which is involved in the formation of neurofibrillary tangles [6]. …”

Section: Introductionmentioning

confidence: 99%

Original Nerve Growth Factor Mimetic Dipeptide GK-2 Restores Impaired Cognitive Functions in Rat Models of Alzheimer’s Disease

et al. 2013

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Dipeptide mimetic of the nerve growth factor (NGF) loop 4, hexamethylenediamide bis-(N-monosuccinyl- glutamyl-lysine) (GK-2), was synthesized at the V.V. Zakusov Scientific Research Institute of Pharmacology of the Russian Academy of Medical Sciences. GK-2 exhibited in vitro neuroprotective activity at nanomolar concentrations, was efficient in animal models of the Parkinson’s disease, ischemic and hemorrhagic stroke, and global cerebral ischemia at doses of 0.01–5 mg/kg (intraperitoneally) and 10 mg/kg (per os). The mnemotropic effects of subchronic intraperitoneal administration of GK-2 on rat models of the Alzheimer’s disease are described in this paper. Dipeptide GK-2 at a dose of 1 mg/kg is found to decrease the habituation deficit induced by the septo-hippocampal pathway transsection and, at a dose of 0.5 mg/kg, to significantly prevent spatial memory impairment in Morris water maze induced by intracerebral injection of streptozotocin. Thus, GK-2, an original dipeptide mimetic of NGF, acts on models of the Alzheimer’s disease upon systemic administration.

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Section: Introductionmentioning

confidence: 99%

Original Nerve Growth Factor Mimetic Dipeptide GK-2 Restores Impaired Cognitive Functions in Rat Models of Alzheimer’s Disease

et al. 2013

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“…3) as presented for mature NGF (or other neurotrophins). In addition, soluble oligomers of -amyloid may also interact with p75 to cause apoptotic signals in neuronal tissue of AD or pre-AD patients (Dechant & Barde, 2002;Diarra et al 2009;Coulson, et al, 2009;Calissano, et al 2010a;2010b;Peng, et al, 2004;Susen & Blochl, 2005). …”

Section: P75 Signalingmentioning

confidence: 99%

Selectivity of Cell Signaling in the Neuronal Response Based on NGF Mutations and Peptidomimetics in the Treatment of Alzheimers Disease

Neet¹,

Mahapatra²,

Mehta³

2011

Alzheimer's Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets

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“…Also, Colostrinin, as well as its constituent nonapeptide not only inhibits aggregation of amyloid b and formation of fibrillar structures but also can dissolve aggregates already formed, acting as a b-sheet breaker [1,2]. Nerve growth factor (NGF) is a neurotrophin that has been shown to exert a number of different, distinguishable effects on neurons, such as survival, growth of fibers, and differentiation of target neurons [3][4][5][6]. NGF plays a critical role in the cortical and hippocampal plasticity, and promotes the survival and functioning of cholinergic neurons.…”

Section: Introductionmentioning

confidence: 99%

“…These neurons are important for memory processes, which are affected in AD. Also, NGF is able to increase neurogenesis of hippocampal neurons [7] and promotes survival of a new neurons in the adult brain [3,8,9]. In AD the decreased synthesis of NGF, the decreased level of TrkA receptors on the neuron surface, and decreased neuronal survival are observed [5,6,[9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

et al. 2014

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Naturally occurring compounds that can act as prosurvival factors and neurite formation stimulants in the conditions of reduced neurotrophins production are important both in neuronal protection and therapy of neurodegenerative disorders. Therefore, the role of proline-rich polypeptide complex (PRP) and its nonapeptide fragment (NP) in the promotion of pheochromocytoma cell line (PC12) survival and neurite outgrowth pathway is presented. It was shown that PRP/NP did not affect the neuronal nitric oxide synthase (nNOS) at the transcriptional and protein level. However, the activity of nNOS and intracellular nitric oxide (NO) concentration was markedly increased after treatment of PC12 cells with peptides. This reaction was inhibited by L-NAME-nNOS inhibitor. It was shown that PRP and NP induce the soluble guanylyl cyclase to release higher amount of cyclic GMP (cGMP), and subsequently, the increased phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) is observed. This effect was abolished by both U0126 (inhibitor of ERK1/2) and also by L-NAME. Reduction of ERK1/2 activity observed in the presence of nNOS inhibitor suggests that its activation is NO-dependent. The presented results shed some light on the mechanism of action of PRP complex. PRP and NP can activate NO/cGMP/ERK1/2 signaling pathway, similarly to nerve growth factor (NGF). The prosurvival action and short fibers formation suggest the role of PRP and NP in neuroprotection and the initiation of neuritogenesis. They can also participate in the amplification of signals controlling the survival and differentiation of neurons effect when the deficit of NGF takes place.

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Does the term ‘trophic’ actually mean anti-amyloidogenic? The case of NGF

Cited by 31 publications

References 90 publications

Original Nerve Growth Factor Mimetic Dipeptide GK-2 Restores Impaired Cognitive Functions in Rat Models of Alzheimer’s Disease

Original Nerve Growth Factor Mimetic Dipeptide GK-2 Restores Impaired Cognitive Functions in Rat Models of Alzheimer’s Disease

Selectivity of Cell Signaling in the Neuronal Response Based on NGF Mutations and Peptidomimetics in the Treatment of Alzheimers Disease

Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

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