Pramipexole prevents neurotoxicity induced by oligomers of beta-amyloid

Uberti, Daniela; Bianchi, Irene; Olivari, Luca; Ferrari-Toninelli, Giulia; Canonico, P.L.; Memo, Maurizio

doi:10.1016/j.ejphar.2007.05.009

Cited by 12 publications

(13 citation statements)

References 15 publications

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“…There is a growing body of evidence suggesting that Aβ peptide toxicity is mediated by free radical damage to cell membranes (Kraus et al, 2007;Uberti et al, 2007). Our present study demonstrates that protofibrillar Aβ causes a significant increase in ROS levels in mouse lymphocytes, hepatocytes and astrocytes (Table 1).…”

Section: Discussionmentioning

confidence: 46%

“…Earlier studies indicate Aβ neurotoxicity in AD resulting from Aβ fibril induced oxidative stress (Yan et al, 1996;Zhang et al, 2007) presumably initiated either directly by Aβ generated free radicals (Kelly et al, 1996;Monji et al, 2002) or indirectly through intracellular production of ROS (Yan et al, 1996). Oligomers of Aβ, protofibril, and fibrillar forms of Aβ are highly neurotoxic (Uberti et al, 2007). Protofibrils appear transiently during Aβ fibrillogenesis (Harper et al, 1997a;Walsh et al, 1997).…”

Section: Introductionmentioning

confidence: 95%

“…However, little is known about the possible neurotoxic effects of in vivo administered Aβ on several other neurotransmitter systems like serotoninergic and noradrenergic. The noncognitive impairments, such as depression and aggressive behavior involved in AD are primarily influenced by the serotoninergic and noradrenergic systems (Dyon-Laurent et al, 1994;Steckler and Sahgal 1995;Uberti et al, 2007;Vanderwolf and Baker 1996).…”

Section: Introductionmentioning

confidence: 99%

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Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism

et al. 2008

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Section: Discussionmentioning

confidence: 46%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism

et al. 2008

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“…In vitro , oxidative stress has been shown to stimulate β-secretase (BACE1) activity, increasing production of pathogenic Aβ 40 and Aβ 42 variants (Tamagno et al, 2008). In turn, small Aβ oligomers act at the mitochondrion to increase production of reactive oxygen species and induce further oxidative damage (Butterfield et al, 2001; Mark et al, 1996; Pappolla et al, 1998; Perluigi et al, 2006; Uberti et al, 2007). Both Aβ and oxidative stress are toxic to neurons (Manelli and Puttfarcken, 1995; Resende et al, 2008), and have been shown to impair memory in an acute, drug-like fashion in the absence of Aβ aggregation (McDonald et al, 1994; McDonald et al, 1996; Sweeney et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Vitamin C deficiency increases basal exploratory activity but decreases scopolamine-induced activity in APP/PSEN1 transgenic mice

Harrison

May

McDonald

2010

Pharmacology Biochemistry and Behavior

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Vitamin C is a powerful antioxidant and its levels are decreased in Alzheimer's patients. Even sub-clinical vitamin C deficiency could impact disease development. To investigate this principle we crossed APP/PSEN1 transgenic mice with Gulo knockout mice unable to synthesize their own vitamin C. Experimental mice were maintained from 6 weeks of age on standard (0.33 g/L) or reduced (0.099 g/L) levels of vitamin C and then assessed for changes in behavior and neuropathology. APP/PSEN1 mice showed impaired spatial learning in the Barnes maze and water maze that was not further impacted by vitamin C level. However, long-term decreased vitamin C levels led to hyperactivity in transgenic mice, with altered locomotor habituation and increased omission errors in the Barnes maze. Decreased vitamin C also led to increased oxidative stress. Transgenic mice were more susceptible to the activity-enhancing effects of scopolamine and low vitamin C attenuated these effects in both genotypes. These data indicate an interaction between the cholinergic system and vitamin C that could be important given the cholinergic degeneration associated with Alzheimer's disease.

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“…Furthermore, apomorphine also exhibits antioxidant effects [139]. Pramipexole, a dopamine agonist used in Parkinson’s disease, has been proposed as an agent to protect cells against formation of oligomers and fibrils of Aβ, which is hypothesized to prevent cell death and reduce the amount of free radicals in neurons (table 1) [140]. …”

Section: Resultsmentioning

confidence: 99%

A Review: Treatment of Alzheimer’s Disease Discovered in Repurposed Agents

Appleby¹,

Nacopoulos²,

Milano³

et al. 2013

Dement Geriatr Cogn Disord

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Background/Aims: Many compounds that have already been approved for alternate diagnoses have been studied in relation to Alzheimer’s disease (AD). The purpose of this review is to summarize these studies and discuss the rationale and benefits of repurposing drugs for AD treatment. Methods: Studies of drugs related to AD treatment that were relevant to a disease-modifying mechanism of action (MOA) and are already approved by the Food and Drug Administration for non-AD diagnoses were collected from PubMed. Results: Many drugs already approved for the treatment of other diseases have been studied in relation to AD treatment. Numerous drugs with known toxicity profiles have the potential to be repurposed as a treatment for AD. Conclusion: Known MOA, toxicology, and pharmacodynamic profiles would accelerate the process and increase the odds of finding a more timely disease-modifying treatment for AD.

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Pramipexole prevents neurotoxicity induced by oligomers of beta-amyloid

Cited by 12 publications

References 15 publications

Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism

Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism

Vitamin C deficiency increases basal exploratory activity but decreases scopolamine-induced activity in APP/PSEN1 transgenic mice

A Review: Treatment of Alzheimer’s Disease Discovered in Repurposed Agents

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