NGF but not BDNF overexpression protects hippocampal LTP from beta-amyloid-induced impairment

Lentiviral-mediated overexpression of nerve growth factor (NGF) prevents beta-amyloid [25–35]-induced long term potentiation (LTP) decline in the rat hippocampus

“…We must also note that in a recent paper by our group we did not observe any visible impact of NGF overexpression on cholinergic transmission in acute brain slices in vitro (Ivanov et al, 2015). This may lead to a conclusion, that in the present in vivo work the NGF protective effect is TrkA-dependent and occurs simultaneously with the hippocampal cholinergic system over-activation.…”

Pin1 mediates Aβ 42 -induced dendritic spine loss

“…Neocortices from AD patients show progressive losses of Pin1 along with synapses and dendritic spines (11) that can be mimicked in cultured neurons (12) or slice preparations (13) treated with multimeric Aβ42. Unexpectedly, germ-line Pin1 KO cortex tissues exhibit increased dendritic spine density and increased LTP in hippocampal slices (6, 10).…”

Cholinergic degeneration in early stages of Alzheimer’s disease: Loss of cholinergic phenotype or loss of cells?

“…However, preliminary transduction of neurons of the dentate gyrus with a vector containing the human NGF gene under the control of a neuron-specific CaMKII promoter allowed to prevent the LTP decline induced by Aβ(25-35). This protective effect was specific for chronically elevated NGF but not BDNF in the hippocampus [47].…”

“…Administration of Aβ(25-35) into the cerebral ventricles or incubation of hippocampal slices with the peptide impaired long-term potentiation (LTP), a form of long-term synaptic plasticity, both in vivo and in slices [46,47]. However, preliminary transduction of neurons of the dentate gyrus with a vector containing the human NGF gene under the control of a neuron-specific CaMKII promoter allowed to prevent the LTP decline induced by Aβ(25-35).…”