In Alzheimer’s disease (AD) there’s a significant atrophy of the basal forebrain cholinergic neurons and losses of synaptic terminations in the cerebral cortex and hippocampus. These neurons depend on the maintenance of synaptic target sites. Since this system plays an important role in higher CNS functions such as attention, learning and memory the cholinergic cellular atrophy and synaptic losses contribute to cognitive impairments in AD and in Down Syndrome (DS) with Alzheimer’s pathology .
Recent investigations have revealed important new vistas on how this system is regulated in health and deregulated in AD. The contributions from the selected group will shed some light on the CNS mechanisms altered in the NGF regulation in AD, how such alterations might provide clues on the existence of a preclinical Alzheimer’s pathology and strategies to remedy the trophic disconnect of basal forebrain cholinergic neurons to ameliorate cognitive impairment in AD and DS.
Drs. Cuello, Mufson, Fahnestock, Granholm, and Mobley will provide clues as to the fundamental mechanisms leading to a trophic disconnect in AD and in DS with AD pathology as well as the derivation of biomarkers revealing alterations of the NGF trophic support in humans. Drs Eriksdotter, Tuszynski and Cattaneo can provide vistas regarding therapeutic strategies to compensate for the loss of NGF trophic support in the above conditions.
In Alzheimer’s disease (AD) there’s a significant atrophy of the basal forebrain cholinergic neurons and losses of synaptic terminations in the cerebral cortex and hippocampus. These neurons depend on the maintenance of synaptic target sites. Since this system plays an important role in higher CNS functions such as attention, learning and memory the cholinergic cellular atrophy and synaptic losses contribute to cognitive impairments in AD and in Down Syndrome (DS) with Alzheimer’s pathology .
Recent investigations have revealed important new vistas on how this system is regulated in health and deregulated in AD. The contributions from the selected group will shed some light on the CNS mechanisms altered in the NGF regulation in AD, how such alterations might provide clues on the existence of a preclinical Alzheimer’s pathology and strategies to remedy the trophic disconnect of basal forebrain cholinergic neurons to ameliorate cognitive impairment in AD and DS.
Drs. Cuello, Mufson, Fahnestock, Granholm, and Mobley will provide clues as to the fundamental mechanisms leading to a trophic disconnect in AD and in DS with AD pathology as well as the derivation of biomarkers revealing alterations of the NGF trophic support in humans. Drs Eriksdotter, Tuszynski and Cattaneo can provide vistas regarding therapeutic strategies to compensate for the loss of NGF trophic support in the above conditions.
