scholarly journals The approval of a disease-modifying treatment for Alzheimer’s disease: impact and consequences for the nuclear medicine community

2021 ◽  
Author(s):  
Valentina Garibotto ◽  
Nathalie L. Albert ◽  
Henryk Barthel ◽  
Bart van Berckel ◽  
Ronald Boellaard ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nuclear Medicine ◽  
Disease Impact ◽  
Disease Modifying ◽  
Disease Modifying Treatment ◽  
Medicine Community ◽  
Nuclear Medicine Community

scholarly journals Disease‐modifying treatment with I2 imidazoline receptor ligand LSL60101 in an Alzheimer's disease mouse model: A Comparative study with donepezil

2021 ◽  
Author(s):  
Foteini Vasilopoulou ◽  
Sergio Rodríguez‐Arévalo ◽  
Andrea Bagán ◽  
Carmen Escolano ◽  
Christian Griñán‐Ferré ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Comparative Study ◽  
Receptor Ligand ◽  
Imidazoline Receptor ◽  
Disease Modifying ◽  
Disease Modifying Treatment

scholarly journals Sodium selenate as a disease-modifying treatment for mild–moderate Alzheimer’s disease: an open-label extension study

2021 ◽  
Vol 3 (2) ◽  
pp. e000223
Author(s):  
Lucy Vivash ◽  
Charles B Malpas ◽  
Christopher M Hovens ◽  
Amy Brodtmann ◽  
Steven Collins ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Progression ◽  
Extension Study ◽  
Sodium Selenate ◽  
Cognitive Measures ◽  
Open Label ◽  
Open Label Extension ◽  
Disease Modifying ◽  
Disease Modifying Treatment

IntroductionSodium selenate is a potential disease-modifying treatment for Alzheimer’s disease (AD) which reduces hyperphosphorylated tau through activation of the protein phosphatase 2A enzyme. We have shown sodium selenate to be safe and well tolerated in a 24-week, phase 2a double-blind placebo-controlled randomised controlled trial (RCT), also reporting sodium selenate reduced neurodegeneration on diffusion-weighted MRI. This study assessed the safety and tolerability of chronic sodium selenate treatment (up to 23 months) in patients with AD who had been enrolled in the RCT. Cognitive measures served as secondary outcomes of potential disease-modification.MethodsAn open-label extension study of sodium selenate (10 mg three times a day) in patients with AD who had completed the previous RCT. Twenty-eight patients were enrolled. Patients were regularly monitored for safety, adverse events (AEs) and protocol compliance. Cognitive tests were administered for measures of disease progression.ResultsSixteen patients were discontinued by the sponsor, and 12 discontinued for other reasons. Treatment duration ranged from 6 to 23 months. The majority of AEs were mild (83%), and 33% were treatment-related. Common treatment-related AEs were alopecia (21%) and nail disorder (32%), which both resolved either prior to or following cessation of treatment. Two serious AEs occurred, which were not treatment-related. Alzheimer’s Disease Assessment Scale—Cognitive Subscale 11 score increased 1.8 points over 12 months.DiscussionChronic sodium selenate treatment is safe and well tolerated in patients with AD. Cognitive measures suggest a slowing of disease progression though this could not be confirmed as the study was not controlled. Further research into sodium selenate as a treatment for AD is warranted.

Taking the Next Steps in the Treatment of Alzheimer's Disease: Disease-Modifying Agents

CNS Spectrums ◽  
2008 ◽  
Vol 13 (S3) ◽  
pp. 11-14
Author(s):  
Stephen Salloway
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Disease Process ◽  
The United States ◽  
Disease Modification ◽  
Disease Modifying ◽  
New Treatment ◽  
Disease Modifying Agents ◽  
Disease Modifying Treatment

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder in the United States and the number of AD patients is increasing at an alarming rate. There is no cure for AD and the currently available treatments are symptomatic, providing only limited effects on disease pathophysiology and progression. An overwhelming need exists for therapies that can slow or halt this debilitating disease process. Disease modification in AD has been defined from patient-focused, regulatory, and neurobiological perspectives. The latter two of these perspectives rely largely on an interruption of the disease process and a clear demonstration of this interruption. As defined by Cummings, a disease-modifying treatment is a “pharmacologic treatment that retards the underlying process of AD by intervening in the neurobiological processes that constitute the pathology and pathophysiology of the disease and lead to cell death or dysfunction.” By this definition, the burden of confirmatory study is placed on any new treatment for which the claim of “disease modification” is to be made (Slide 1).

Eligibility for disease-modifying treatment in Alzheimer's disease: Evidence from an observational study over 4 years

2021 ◽  
Vol 429 ◽  
pp. 118982
Author(s):  
Salvatore Caratozzolo ◽  
Luca Rozzini ◽  
Maura Cosseddu ◽  
Rosanna Turrone ◽  
Silvia Compostella ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Observational Study ◽  
Disease Modifying ◽  
Disease Modifying Treatment

scholarly journals Oxidative Stress in Alzheimer’s Disease: Why Did Antioxidant Therapy Fail?

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Torbjörn Persson ◽  
Bogdan O. Popescu ◽  
Angel Cedazo-Minguez
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Clinical Studies ◽  
Current Knowledge ◽  
The Elderly ◽  
Antioxidant Treatment ◽  
Disease Modifying ◽  
Disease Modifying Treatment

Alzheimer’s disease (AD) is the most common form of dementia in the elderly, with increasing prevalence and no disease-modifying treatment available yet. A remarkable amount of data supports the hypothesis that oxidative stress is an early and important pathogenic operator in AD. However, all clinical studies conducted to date did not prove a clear beneficial effect of antioxidant treatment in AD patients. In the current work, we review the current knowledge about oxidative stress in AD pathogeny and we suggest future paths that are worth to be explored in animal models and clinical studies, in order to get a better approach of oxidative imbalance in this inexorable neurodegenerative disease.

Emerging prospects for the disease-modifying treatment of Alzheimer's disease

2005 ◽  
Vol 69 (7) ◽  
pp. 1001-1008 ◽  
Author(s):  
Lary C. Walker ◽  
Chris C. Ibegbu ◽  
Charles W. Todd ◽  
Harriet L. Robinson ◽  
Mathias Jucker ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Modifying ◽  
Disease Modifying Treatment

Cognitive symptoms of Alzheimer’s disease: clinical management and prevention

BMJ ◽  
2019 ◽  
pp. l6217 ◽  
Author(s):  
Elizabeth Joe ◽  
John M Ringman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Acetylcholinesterase Inhibitors ◽  
Amyloid Cascade Hypothesis ◽  
Prodromal Ad ◽  
Disease Modifying ◽  
Medical Foods ◽  
Disease Modifying Treatment ◽  
Amyloid Cascade

ABSTRACTAlzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of amyloid β in the form of extracellular plaques and by intracellular neurofibrillary tangles, with eventual neurodegeneration and dementia. There is currently no disease-modifying treatment though several symptomatic medications exist with modest benefit on cognition. Acetylcholinesterase inhibitors have a consistent benefit across all stages of dementia; their benefit in mild cognitive impairment and prodromal AD is unproven. Memantine has a smaller benefit on cognition overall which is limited to the moderate to severe stages, and the combination of a cholinesterase inhibitor and memantine may have additional efficacy. Evidence for the efficacy of vitamin E supplementation and medical foods is weak but might be considered in the context of cost, availability, and safety in individual patients. Apparently promising disease-modifying interventions, mostly addressing the amyloid cascade hypothesis of AD, have recently failed to demonstrate efficacy so novel approaches must be considered.

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