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Impairment of the nerve growth factor pathway driving amyloid accumulation in cholinergic neurons the incipit of the Alzheimer's disease story?

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Neural Regeneration Research 2016年第10期11卷 1553-1556页

作者： Viviana Triaca pietro calissano European Brain Research Institute (EBRI)/R.L. Montalcini Foundation and Institute of Cell Biology and Neuroscience National Research Council (IBCN-CNR)

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） al- terations 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 neuro- trophins 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 sep- to-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.

关键词： Alzheimer's disease onset NGF pathway disturbances intraneuronal amyloid generation andrelease basal forebrain cholinergic neurons

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A long story for a short peptide:therapeutic efficacy of a cleavagespecific tau antibody

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Neural Regeneration Research 2021年第12期16卷 2417-2419页

作者： Giuseppina Amadoro Valentina Latina pietro calissano Institute of Translational Pharmacology(IFT)-National Research Council(CNR) Via Fosso del Cavaliere 10000133-RomeItaly(Amadoro G)European Brain Research Institute(EBRI)Viale Regina Elena 29500161-RomeItaly

Tau is the prime participant in the Alzheimer’s disease(AD) neurodegeneration:AD,the main cause of dementia in elderly people,is a multifactorial neurodegenerative disorder characterized by a long prodromal phase(starting more than two decades before clinical symptoms appear)with brain accumulation/misfolding of amyloidβ(Aβ)in insoluble amyloid plaques and of tau protein in neurofibrillary tangles.

关键词： tau Aβ Alzheimer

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