Alzheimers disease (AD) is the most common cause of dementia in the elderly. AD is a neurodegenerative disease characterized by the loss of cognitive functioning - thinking, remembering and reasoning- and behavioral abilities to such an extent that it interferes with a persons daily life and activities. The neuropathological hallmarks of AD include amyloid plaques and neurofibrillary tangles, which lead to neuronal death. Studies in animal models of AD have shown that p75NTR contributes to amyloid β-induced neuronal damage. In humans with AD, increases in p75NTR expression relative to TrkA have been suggested to be responsible for the loss of cholinergic neurons. Increases in proNGF in AD  indicate that the Neurotrophin environment is favorable for p75NTR/sortilin signaling and supports the theory that age-related neural damage is facilitated by a shift toward proNGF-mediated signaling. A recent study found that activation of Ngfr signaling in astroglia of Alzheimers disease mouse model enhanced neurogenesis and reduced two hallmarks of Alzheimers disease. This study also found that NGFR signaling in humans is age-related and correlates with proliferative potential of neural progenitors.