It is possible, that the chronic overexpression of TGF-β results in physiological artifacts leading to contradictory data on the neuroprotective role of TGF-β1 in AD as a modest increase in astroglial TGF-β1 production in aged transgenic mice expressing the human beta-amyloid precursor protein resulted in a reduction in the number of parenchymal amyloid plaques in the hippocampus and cerebral cortex, and decreased the number of dystrophic neurites [119]. Here, TGFB1 is linked to Alzheimer disease.