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

O4-11-02: Disease Modifying Therapy by the Infusion of an Anti-Conformational Monoclonal Antibody in an Ab and TAU 3XTG Mouse Model of Alzheimer's Disease

2016 ◽  
Vol 12 ◽  
pp. P360-P360 ◽  
Author(s):  
Fernando Goni ◽  
Krystal Herline ◽  
Mitchell Marta-Ariza ◽  
Allal Boutajangout ◽  
Pankaj D. Mehta ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Monoclonal Antibody ◽  
Mouse Model ◽  
Disease Modifying Therapy ◽  
Model Of Alzheimer’S Disease ◽  
Disease Modifying

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).

scholarly journals The Liver X Receptor Ligand T0901317 Decreases Amyloid β Productionin Vitroand in a Mouse Model of Alzheimer's Disease

2004 ◽  
Vol 280 (6) ◽  
pp. 4079-4088 ◽  
Author(s):  
Radosveta P. Koldamova ◽  
Iliya M. Lefterov ◽  
Matthias Staufenbiel ◽  
Darren Wolfe ◽  
Shaohua Huang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Liver X Receptor ◽  
Receptor Ligand ◽  
Model Of Alzheimer’S Disease

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
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