Abstract
BackgroundAlzheimer’s disease (AD) and diabetes mellitus (DM) often coexist in patients because having one of these conditions increases risk for the other. These two diseases share several pathophysiological mechanisms, such as specific inflammatory signaling pathways, oxidative stress, and cell apoptosis. It is still unclear exactly which mechanisms associated with DM are responsible for increased AD risk. Studies have found that even transient elevation of brain Aβ levels can allow T2DM to slightly disrupt the neural milieu in a way that encourages pathologies associated with the onset of memory deficits and AD. A recent study argues that a potential common pathogenetic mechanism underlying both DM and AD is evidenced by the cooccurrence of amyloid brain legions and deposits containing both tau and Aβ in pancreatic β cells. Given these links, an investigation detailing disease mechanisms as well as treatment options for patients with cooccurring DM and AD is urgently needed. The biological effects of resveratrol relevant to DM and AD treatment include its abilities to modulate oxidative stress and reduce inflammation. A rat model of DM and concomitant AD was created for this study using intraperitoneal injection of streptozotocin and hippocampal injection of Aβ1–40 to characterize resveratrol’s potential protective action.ResultsResveratrol significantly increased the Sirt1 expression, inhibited the memory impairment, the increased acetylcholinesterase, malondialdehyde, interleukin-1β and interleukin 6 levels, and the decreased levels of choline acetyltransferase (ChAT), superoxide dismutase (SOD), and glutathione in this rat model of diabetes and concomitant AD. The Sirt 1 inhibitor EX527 partially reversed the effects of resveratrol.ConclusionThis study suggests that resveratrol may have a neuroprotective action through activation of Sirt1 signaling in diabetes and AD with concurrent onset.
Highlights
Alzheimer’s disease (AD) is a disorder involving selective central nervous system degeneration, including neuron loss and gradual development of amyloid plaques and neurofibrillary tangles (Iwatsubo, 2000)
Escape latency and escape distance in rats treated with both resveratrol and EX527 were significantly longer compared to rats treated with resveratrol alone (P < 0.05) (Figure 2), indicating that the Sirt1 inhibitor EX527 can partially reverse the effects of resveratrol
The percentage of time (Figure 3A) and percentage of distance swum (Figure 3B) in rats receiving both resveratrol and EX527 were both significantly less compared to rats receiving only resveratrol (P
Summary
Alzheimer’s disease (AD) is a disorder involving selective central nervous system degeneration, including neuron loss and gradual development of amyloid plaques and neurofibrillary tangles (Iwatsubo, 2000). Alzheimer’s disease (AD) and diabetes mellitus (DM) often coexist in patients because having one of these conditions increases risk for the other These two diseases share several pathophysiological mechanisms, such as specific inflammatory signaling pathways, oxidative stress, and cell apoptosis. It is still unclear exactly which mechanisms associated with DM are responsible for increased AD risk. A recent study argues that a potential common pathogenetic mechanism underlying both DM and AD is evidenced by the cooccurrence of amyloid brain legions and deposits containing both tau and Aβ in pancreatic β cells Given these links, an investigation detailing disease mechanisms as well as treatment options for patients with cooccurring DM and AD is urgently needed. A rat model of DM and concomitant AD was created for this study using intraperitoneal injection of streptozotocin and hippocampal injection of Aβ1–40 to characterize resveratrol’s potential protective action
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