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| 1 | Impairment of the nerve growth factor pathway driving amyloid accumulation in cholinergic neurons the incipit of the Alzheimer's disease story?显示文摘The current idea behind brain pathology is that disease is initiated by mild disturbances of common physiological processes. Overtime, the disruption of the neuronal homeostasis will determine irreversible degeneration and neuronal apoptosis. This could be also true in the case of nerve growth factor(NGF) alterations in sporadic Alzheimer's disease(AD), an age-related pathology characterized by cholinergic loss, amyloid plaques and neurofibrillary tangles. In fact, the pathway activated by NGF, a key neurotrophin for the metabolism of basal forebrain cholinergic neurons(BFCN), is one of the first homeostatic systems affected in prodromal AD. NGF signaling dysfunctions have been thought for decades to occur in AD late stages, as a mere consequence of amyloid-driven disruption of the retrograde axonal transport of neurotrophins to BFCN. Nowadays, a wealth of knowledge is potentially opening a new scenario: NGF signaling impairment occurs at the onset of AD and correlates better than amyloid load with cognitive decline. The recent acceleration in the characterization of anatomical, functional and molecular profiles of early AD is aimed at maximizing the efficacy of existing treatments and setting novel therapies. Accordingly, the elucidation of the molecular events underlying APP metabolism regulation by the NGF pathway in the septo-hippocampal system is crucial for the identification of new target molecules to slow and eventually halt mild cognitive impairment(MCI) and its progression toward AD. | Viviana Triaca Pietro Calissano | 2016 | Neural Regeneration Research2016，11，10： | 5 |
| 2 | Nerve growth tactor as a paradigm of neurotrophins related to Alzheimer's dis- ease 显示文摘 | Calissano P Matrone C Amadoro G | 2010 | DevNeurobiol2010，70，5： | 1 |
| 3 | Glutamate neurotox- ieity,oxidative stress and mitoehondria 显示文摘 | Atlante A Calissano P Bobba A | 2001 | FEBS Letters2001，497，1： | 1 |
| 4 | Cytochrome c is released from mitochondria in a reactive oxygen species(ROS)-dependentfashion and can operate as a ROS scavenger and as a respiratory substrate in cerebellarneurons undergoing excitotoxic death显示文摘 | Atlante A Calissano P Bobba A | 2000 | J Biol Chem2000，275，37： | 1 |
| 5 | Phosphorylation of the Brn3a transcription factor is modulated during differentiation and regulates its functional activity显示文摘 | Faulkes D Latchman DS | 2005 | Brain Res Mol Brain Res2005，141，1： | 1 |
| 6 | Nerve growth factor and Alzheimer's disease: new facts for an old hypothesis显示文摘 | Cattaneo A Calissano P | 2012 | Mol Neurobiol2012，46，3： | 1 |
| 7 | Apoptosis and in vitro Alzheimer disease neuronal models显示文摘 | CALISSANO P MATRONE C AMADORO G | 2009 | Commun Integr Biol2009，2，2： | 1 |
| 8 | Apoptosis and in vitru Alzheirner disease neuranal models显示文摘 | Calissano P Matrone C Amacloro G | 2009 | Commun lntegr Biol2009，2，2： | 1 |
| 9 | Lithium induces apoptosis in immature cerebellar granule cells but promotes survival of mature neurons显示文摘 | D'Mello S R Anelli R Calissano P | | 0，，02： | 1 |
| 10 | Apoptosis and in vitro Alzheimer disease neuronal models显示文摘 | Calissano P Matrone C Amadoro G | 2009 | Commun Integr Biol2009，2，2： | 1 |
| 11 | IL4-589C/T polymorphism and IgE levels in severe malaria显示文摘 | Verra F Luoni G Calissano C | 2004 | Acta Trop2004，90，2： | 1 |
| 12 | Apoptosis and in vitro Alzheimer disease neuronal models显示文摘 | Calissano P Matrone C Amadoro G | 2009 | Commun Integr Biol2009，2，2： | 1 |
| 13 | Glutamate neurotoxicity,oxidative stress and mitochondria显示文摘 | Atlante A Calissano P Bobba A | | 0，，： | 1 |
| 14 | Caspase-dependent alteration of the ADP/ATP translocator triggers the mitochondrial perme-ability transition which is not required for the low-potassium-dependent apoptosis of cerebellar granule cells 显示文摘 | Atlante A Bobba A de Bari L Fontana F Calissano P Marra E Passarella S | 2006 | J Neurochem2006，97，4： | 1 |
| 15 | Glutamate neurotoxicity, oxidative stress and mitochondria显示文摘 | Atlante A Calissano P Bobba A | 2001 | FEBS Lett2001，497，1： | 1 |
| 16 | Cytochrome c is released from mitochondria in a reactive oxygen species(ROS)-dependent fashion and can operate as a ROS scavenger and as a respiratory substrate in cerebellar neurons undergoing excitotoxic death 显示文摘 | ATLANTE A CALISSANO P BOBBA A | 2000 | Journal of Biological Chemistry2000，275，37： | 1 |
| 17 | In vitro cultured neurons for molecular studies correlating apoptosis with events related to Alzheimer disease显示文摘 | Canu N Calissano P | 2003 | Cerebellum2003，2，4： | 1 |
| 18 | The brain protein S-100 ab induces apoptosis in PC12 cells显示文摘 | Mariggio MA Fulle S Calissano P | 1994 | Neuroscience1994，60，： | 1 |
| 19 | Glutamate neurotoxicity, oxidative stress and mitochondria显示文摘 | Anna Atlante Pietro Calissano Antonella Bobba Sergio Giannattasio Ersilia Marra Salvatore Passarella | 2001 | FEBS Letters2001，，1： | 1 |
| 20 | Glutamate neurotoxieity, oxidative stress and mitochondria显示文摘 | Atlante A Calissano P Bobba A | 2001 | FEBS Lett2001，497，1： | 1 |
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