Late-onset Alzheimer’s disease (LOAD) is a long-enduring neurodegenerative disease that progresses for decades before the symptoms of cognitive decline and loss of executive function are measurable. Amyloid deposits among other pathological changes, tau hyperphosphorylation, synapse loss, microglia and astroglia activation, and hippocampal atrophy are among the pathological hallmarks of the disease. These are present in the brain before memory complaints are reported and an AD diagnosis is made.
View Article and Find Full Text PDFThe basic strategy for focusing exclusively on genetically identified targets for intervening in late life dementias was formulated 30 years ago. Three decades and billions of dollars later, all efforts at disease-modifying interventions have failed. Over that same period, evidence has accrued pointing to dementias as late-life clinical phenotypes that begin as midlife pathologies.
View Article and Find Full Text PDFScientificWorldJournal
February 2011
Within days of each other, Pfizer, Merck, and GlaxoSmithKline announced that they will focus on a few therapeutic areas only and abandon others entirely. Pfizer alone will close well over a hundred drug development projects that have reached two-thirds of the way to launch. The programs are deemed to be too risky and not lucrative enough for Big Pharma in the current climate.
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