Ludis Morales

TL;DR: The aim of this paper is to present various well-known dietary polyphenols and their mechanisms of neuroprotection with an emphasis on Alzheimer’s disease, Parkinson's disease, and amyotrophic lateral sclerosis.

TL;DR: This review will focus on astrocytic activities that can both protect and endanger neurons, and discuss how manipulating these functions provides a novel and important strategy to enhance neuronal survival and improve the outcome following brain injury.

TL;DR: It is hypothesized that since an imbalance between the NOS isoforms and endothelin-1 (ET-1), a human gene that encodes for blood vessel constriction, can cause antioxidant system insufficiency, the brain lesions and the downstream progression of brain pathology and dementia in AD should be delayed or minimized by using pharmacological intervention with NO donors and/or NO suppressors.

TL;DR: The mechanisms by which polyphenols and endogenous antioxidants can produce protection against oxidative stress are reviewed, including: scavenging nitrogen and oxygen reactive species, regulation of signaling pathways associated with cell survival and inflammation, and inhibition of synphilin-1 and alpha-synuclein aggregation.

TL;DR: A large body of evidence indicates that sporadic, late-onset AD results from a vascular etiology by briefly reviewing mitochondrial damage and vascular risk factors associated with the disease and then discusses the cerebral microvascular changes reason for the energy failure that occurs in normal aging and, to a much greater extent, AD.