Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: a randomized controlled trial.

Incidence of a fracture, particularly in the hip joint, is high in elderly women with Parkinson's disease (PD), and this is due to the immobilization-induced bone resorption and vitamin D deficiency with reduced bone mineral density (BMD). The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2-year follow-up period was studied. At baseline, both groups of patients had low BMD with high levels of serum-ionized calcium and urinary deoxypyridinoline (D-Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10-0.85). The number of hip fracture per 1,000 patient-years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D-Pyr levels decreased significantly during the follow-up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures.     

Retraction: ‘Sunlight exposure is important for preventing hip fractures in patients with Alzheimer's disease,Parkinson's disease,or stroke’ by J. Iwamoto,T. Takeda and H. Matsumoto

The above article from Acta Neurologica Scandinavica, published online on 18 June 2011 in Wiley Online Library ( http://wileyonlinelibrary.com ) and in Volume 125, pp. 279‐284, has been retracted by agreement between the authors, the Journal Editor‐in‐Chief Elinor Ben‐Menachem and John Wiley & Sons Ltd. The Retraction has been agreed due to extensive duplication of previously published material on the part of Dr Sato, who has acknowledged full responsibility. Dr. Iwamoto would like to note the following information related to this retraction:

• Dr. Sato admitted that he was solely involved in the scientific misconducts.
• I did not actually participate in Dr. Sato's studies. I am an honorary author of Sato's Papers.
• When I was preparing the Subject Paper in the year 2012, I clearly was unaware of the fact Dr. Sato was involved in scientific misconducts.

REFERENCES Sato Y, Iwamoto J, Kanoko T, Satoh K. Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in hospitalized, elderly women with Alzheimers disease: a randomized controlled trial. J Bone Miner Res. 2005;20:1327‐1333. Sato Y, Iwamoto J, Honda Y. Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in Parkinson's disease. Parkinsonism Relat Disord. 2011;17:22‐26. Sato Y, Metoki N, Iwamoto J, Satoh K. Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in stroke patients. Neurology. 2003;61:338‐342. Iwamoto J, Takeda T, Matsumoto H. Sunlight exposure is important for preventing hip fractures in patients with Alzheimer's disease, Parkinson's disease, or stroke. Acta Neurol Scand. 2012;125:279‐284.     

Efficacy and safety of Cerebrolysin in moderate to moderately severe Alzheimer’s disease: results of a randomized,double‐blind,controlled trial investigating three dosages of Cerebrolysin

Background: Cerebrolysin is a neuropeptide preparation mimicking the effects of neurotrophic factors. This subgroup analysis assessed safety and efficacy of Cerebrolysin in patients with moderate to moderately severe Alzheimer’s disease (AD) (ITT data set: N = 133; MMSE: 14–20) included in a dose‐finding study (ITT data set: N = 251; MMSE: 14–25). Results of the mild AD subgroup (ITT data set: N = 118; MMSE: 21–25) are also presented. Methods: Patients with AD received 100 ml IV infusions of Cerebrolysin (10, 30 or 60 ml diluted in saline; N = 32, 34 and 35, respectively) or placebo (saline; N = 32) over twelve weeks (5 days per week for 4 weeks and 2 days per week for another 8 weeks). Primary efficacy criteria ADAS‐cog+ (Alzheimer’s Disease Assessment Scale Cognitive Subpart Modified) and CIBIC+ (Clinical Interview‐based Impression of Change with Caregiver Input) were assessed 24 weeks after baseline. Results: At week 24, Cerebrolysin improved the global clinical function significantly with all three dosages and induced significant improvements in cognition, initiation of activities of daily living (ADL) and neuropsychiatric symptoms at 10‐, 30‐ and 60‐ml doses, respectively. Treatment effects on total ADL and other secondary parameters (MMSE, Trail‐making test) were not significant. Cerebrolysin was safe and well tolerated. Conclusions: These results demonstrate the efficacy of Cerebrolysin in moderate to moderately severe AD, showing dose‐specific effects similar to those reported for patients with mild to moderate AD. The benefits of Cerebrolysin in advanced AD need to be confirmed in larger trials.     

Rotigotine improves restless legs syndrome: A 6‐month randomized,double‐blind,placebo‐controlled trial in the United States

This randomized, double‐blinded, placebo‐controlled trial (NCT00135993) assessed efficacy and safety of the dopamine agonist rotigotine in the treatment of idiopathic restless legs syndrome (RLS) over a 6‐month maintenance period. A total of 505 eligible participants with moderate to severe RLS (IRLS sum score ≥ 15) were randomly assigned to five groups to receive either placebo or rotigotine (0.5, 1, 2, or 3 mg/24 hr) delivered by once‐daily transdermal patch (fixed‐dose regimen). The two co‐primary efficacy parameters decreased from baseline to end of maintenance in IRLS sum score and in clinical global impressions (CGI‐1) score. On both primary measures, 2 and 3 mg/24 hr rotigotine was superior to placebo (P < 0.001). Adjusted treatment differences to placebo for the IRLS sum score were ?4.5 (95% CI: ?6.9, ?2.2) for 2 mg/24 hr rotigotine, ?5.2 (95% CI: ?7.5, ?2.9) for 3 mg/24 hr rotigotine, and for CGI item 1 ?0.65 (95% CI: ?1.0, ?0.3) and ?0.9 (95% CI: ?1.3, ?0.5) for the 2 and 3 mg/24 hr doses, respectively. Skin reactions (27%) and known dopaminergic side effects such as nausea (18.1%) and headache (11.6%) were mostly mild or moderate in rotigotine subjects. Rotigotine transdermal patches releasing 2 to 3 mg/24 hr significantly reduced the severity of RLS symptoms. Treatment efficacy was maintained throughout the 6‐month double‐blind period. © 2010 Movement Disorder Society     

Escitalopram for agitation in Alzheimer's disease (S-CitAD): Methods and design of an investigator-initiated,randomized, controlled,multicenter clinical trial

IntroductionAlzheimer's disease (AD) is a disabling, common cause of dementia, and agitation is one of the most common and distressing symptoms for patients with AD. Escitalopram for agitation in Alzheimer's disease (S-CitAD) tests a novel, clinically derived therapeutic approach to treat agitation in patients with AD.MethodsS-CitAD is a NIH-funded, investigator-initiated, randomized, multicenter clinical trial. Participants receive a structured psychosocial intervention (PSI) as standard of care. Participants without sufficient response to PSI are randomized to receive 15 mg escitalopram/day or a matching placebo in addition to PSI. Primary outcome is the Modified Alzheimer's Disease Cooperative Study - Clinical Global Impression of Change (mADCS-CGIC).DiscussionS-CitAD will provide information about a practical, immediately available approach to treating agitation in patients with AD. S-CitAD may become a model of how to evaluate and predict treatment response in patients with AD and agitation as a neuropsychiatric symptom (ClinicalTrials.gov Identifier: NCT03108846).