1,721,032 research outputs found
Amyloid-directed monoclonal antibodies for the treatment of Alzheimer's disease: the point of no return?
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Are NSAIDs useful to treat Alzheimer's disease or mild cognitive impairment?
No full textSeveral epidemiological studies suggest that long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) may protect subjects carrying one or more ε4 allele of the apolipoprotein E (APOE ε4) against the onset of Alzheimer’s disease (AD). The biological mechanism of this protection is not completely understood and may involve the anti-inflammatory properties of NSAIDs or their ability of interfering with the β-amyloid (Aβ) cascade. Unfortunately, long-term, placebo-controlled clinical trials with both non-selective and cyclooxygenase-2 (COX-2) selective inhibitors in mild-to-moderate AD patients produced negative results. A secondary prevention study with rofecoxib, a COX-2 selective inhibitor, in patients with mild cognitive impairment was also negative. A primary prevention study (ADAPT trial) of naproxen (a non-selective COX inhibitor) and celecoxib (a COX-2 selective inhibitor) in cognitively normal elderly subjects with a family history of AD was prematurely interrupted for safety reasons after a median period of treatment of 2 years. Although both drugs did not reduce the incidence of dementia after two years of treatment, a 4-year follow up assessment surprisingly revealed that subjects previously exposed to naproxen were protected from the onset of AD by 67% compared to placebo. Thus, it could be hypothesized that the chronic use of NSAIDs may be beneficial only in the very early stages of the AD process in coincidence of initial Aβ deposition, microglia activation and consequent release of pro-inflammatory mediators. When the Aβ deposition process is already started, NSAIDs are no longer effective and may even be detrimental because of their inhibitory activity on chronically activated microglia that on long-term may mediate Aβ clearance. The research community should conduct long-term trials with NSAIDs in cognitively normal APOE ε4 carriers
Different effects of atropine and cimetropium bromide on gastric emptying of liquids and antroduodenal motor activity in man.
No full textAtropine (1 mg intravenously) and a new antimuscarinic compound, cimetropium bromide (5 mg intravenously), as well as placebo (physiological saline) were tested for their effects on gastric emptying and antroduodenal motility in healthy humans. In a first single-blind cross-over study, the emptying rate was assessed in 12 subjects by measuring paracetamol absorption. In a second single-blind parallel-group study, antroduodenal motor activity was measured in 20 subjects through four perfused open tip catheters with orifices positioned in the antroduodenal region. Atropine, unlike cimetropium bromide, significantly delayed gastric emptying. Antral and duodenal motility index was reduced significantly by atropine, but not by cimetropium bromide. Heart rate significantly increased only after atropine. Three subjects taking atropine complained of dry mouth and one of blurred vision. In conclusion, the results of these studies show that atropine, unlike cimetropium bromide, strongly inhibits gastric emptying of liquids and reduces antroduodenal motor activity in man
Nutraceutical properties of Mediterranean diet and cognitive decline: possible underlying mechanisms
No full textAmyloid-based immunotherapy for Alzheimer's disease in the time of prevention trials: the way forward
No full textMechanism of action of hexarelin and GHRP-6: analysis of the involvement of GHRH and somatostatin in the rat.
No full textBapineuzumab: anti-β-amyloid monoclonal antibodies for the treatment of Alzheimer's disease
No full textAmyloid-based immunotherapy for Alzheimer's disease in the time of prevention trials: the way forward.
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