This trial is evaluating whether Canakinumab will improve 1 primary outcome and 6 secondary outcomes in patients with Alzheimer Disease. Measurement will happen over the course of Baseline and at 12 weeks.
This trial requires 90 total participants across 2 different treatment groups
This trial involves 2 different treatments. Canakinumab is the primary treatment being studied. Participants will all receive the same treatment. Some patients will receive a placebo treatment. The treatments being tested are in Phase 2 and have already been tested with other people.
About 8.1 million people have Alzheimer's disease. Half of adults aged 65 years and older and 20% of adults younger than age 65 who have Alzheimer's disease died by July 2013. In the United States, the life span for the disease is only a few years. One-fourth of people who die from the disease live 5 years or less.
Results from a recent paper provides baseline estimates of common treatment options for elderly patients with AD in Japan, revealing significant differences between previous estimates of common treatments for the disease, especially those for patients with severe AD.
AD affects 10 to 15 per 1000 elderly citizens of the developed world, is the most common type of dementia and the main cause of death in those over 80 years old. AD is a progressive dementia leading to cognitive impairment and finally, death.\n
There is no known infectious cause of AD; however, some genetic risk factors are known. People with APOE-psuedomineralocorticoid receptor APOE4 allele have a 10- to 35-fold increase in the risk of AD compared to the wild type. The genetic risk factor is different for familial and sporadic AD. Genetic factors influencing AD risk may include factors that cause the neurodegenerative pathology of AD, such as inflammation, oxidative stress or a dysregulated complement system. Alternatively, some risk factors may work indirectly via effects on dementia. There are various possible mechanisms, including epigenetic mechanisms and changes to the immune system.
Symptoms must be supported by physical evidence of disease in order for an eventual diagnosis to be made. In cases where dementia was only suspected, many patients developed the symptoms of a vascular origin and may have only been a precursor or early stage of AD. AD is typically diagnosed via an autopsy, so all deaths of both dementia and cognitively normal subjects must have post-mortem histopathology. All subjects with signs of dementia in this study were examined and diagnosed with Alzheimers, which were assessed at autopsy.
Alzheimer disease cannot be cured despite extensive scientific investigations that have generated many hypotheses and clinical trials that would tend to disprove the hypothesis. However, early detection and aggressive treatment can reduce morbidity and mortality and increase quality of life. The goal of these guidelines is to support physicians in identifying those with Alzheimer's disease and to help their patients and families make informed treatment decisions regarding potential cures.
The average age people actually are diagnosed with Alzheimer's disease is 77. In the US, more men are diagnosed with Alzheimer's at younger ages than women – especially among the oldest (greatest 85+). Results from a recent clinical trial may reflect cultural perceptions of the [Alzheimer's disease] pathology and early diagnosis.
The use of canakinumab was associated with a considerable reduction in the use of all other medications, especially antiepileptics and antipsychotics; however, the use of anticholinergics increased with canakinumab. The use of biologics was most frequently prescribed in combination with other pharmacological treatments. The findings indicated that the canakinumab is typically used in combination with other medications. However, further research is required to identify other conditions for which canakinumab has been shown to be effective.
Significant and transient clinical and biochemical effects of canakinumab were observed in a cohort of patients with AD and a variety of baseline clinical and biomarkers, including mild and asymptomatic elevations of liver enzymes. The overall frequency and severity of side effects was higher than previously reported for canakinumab in preclinical studies. ClinicalTrials.gov (https://clinicaltrials.gov) Identifier: NCT01689958.
Symptoms in about 70% of patients with AD can be cured by canakinumab and that such remission would last for one year. This response to canavinumab is not due to drug accumulation.
There are multiple clinical trials in progress involving canakinumab for the treatment of AD. One of these trials compares canakinumab with an existing approved therapy, atenolol, for treating patients at high risk for developing a potentially life-threatening cardiovascular disease.
Genetic factors have a role in pathogenesis of AD, but they are not responsible for the majority of familial AD. AD is the most common type of dementia in people with the APOE e4 genotype. Genetic factors do not account for the differences in the incidence of AD between whites and Africans.