Abstract
GENERAL COMMENTARY article Front. Neurol., 18 December 2014Sec. Neuropharmacology https://doi.org/10.3389/fneur.2014.00276
Highlights
A commentary on Successful therapies for Alzheimer’s disease: why so many in animal models and none in humans? by Franco R, Cedazo-Minguez A
One of the histopathological hallmarks of the disease is the presence of amyloid beta (Aβ) plaques; it seems that soluble oligomers, called Aβ-derive-diffusible-ligands (ADDLs), are the really toxic species involved in the pathogenesis of Alzheimer’s disease (AD) [2]
NEUROINFLAMMATION AND NEURODEGENERATION, TWO OF THE CHARACTERS IN THE PROGRESSION OF THE DISEASE The neuronal loss observed in the AD brains, as occurs in other neurodegenerative diseases, is produced mainly by apoptosis [13, 14]
Summary
A commentary on Successful therapies for Alzheimer’s disease: why so many in animal models and none in humans? by Franco R, Cedazo-Minguez A. ALZHEIMER’S DISEASE AND AMYLOID BETA Defining characteristics of Alzheimer’s disease (AD) are memory defects, synaptic alterations, presence of neuroinflammatory mediators, and a progressive neurodegeneration. One of the histopathological hallmarks of the disease is the presence of amyloid beta (Aβ) plaques; it seems that soluble oligomers, called Aβ-derive-diffusible-ligands (ADDLs), are the really toxic species involved in the pathogenesis of AD [2]. NEUROINFLAMMATION AND NEURODEGENERATION, TWO OF THE CHARACTERS IN THE PROGRESSION OF THE DISEASE The neuronal loss observed in the AD brains, as occurs in other neurodegenerative diseases, is produced mainly by apoptosis [13, 14].
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