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β/A4‐Amyloid increases nerve growth factor production in rat primary hippocampal astrocyte cultures
Author(s) -
SchulteHerbrüggen O.,
Hamker U.,
Meske V.,
DankerHopfe H.,
Ohm T.G.,
Hellweg R.
Publication year - 2007
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2007.05.010
Subject(s) - nerve growth factor , cholinergic neuron , neurotrophin , hippocampal formation , basal forebrain , cholinergic , neuroprotection , astrocyte , endocrinology , neuroscience , medicine , neurotrophic factors , neurotrophin 3 , amyloid precursor protein , alzheimer's disease , biology , brain derived neurotrophic factor , receptor , central nervous system , disease
Nerve growth factor (NGF), a member of the neurotrophin family, is an essential mediator of neuronal activity and synaptic plasticity of basal forebrain cholinergic neurons (BFCN). In processes of chronic degeneration of BFCN like in Alzheimer's disease (AD), characterized among others by amyloid containing plaques, NGF has been shown to improve cognitive decline and rescue BFCN but also to reduce survival of hippocampal neurons via p75 neurotrophin receptor (p75). Little is known about the mechanisms of NGF regulation in glial cells under pathological conditions in AD. This study investigates the influence of amyloid administration on the NGF protein secretion in rat primary hippocampal astrocytes. Astrocytes were stimulated with “aged” β/A4‐Amyloid (1‐40), and NGF was measured in different fractions, such as supernatant, vesicles, and cytosol fraction. Treatment with amyloid at a final concentration of 10 μM for 72 h led to increased NGF protein levels up to 30‐fold increase compared to unstimulated controls. This observation may be an endogenous neuroprotective mechanism possibly contributing to a delay of amyloid‐dependent loss of cholinergic neurons or contribute to accelerated neuronal death by activation of p75 within Alzheimer pathology.