Aβ Immunotherapy: Lessons Learned for Potential Treatment of Alzheimer’s Disease

2005 ◽  
Vol 2 (5) ◽  
pp. 255-260 ◽  
Author(s):  
Dale B. Schenk ◽  
Peter Seubert ◽  
Michael Grundman ◽  
Ron Black
2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 850-850
Author(s):  
Nicole Dawson ◽  
Heather Menne

Abstract The National Institute on Aging recognizes the importance of identifying promising non-pharmacological interventions (NPI) to promote health in individuals with Alzheimer’s disease and related dementias. Several systematic reviews have been completed investigating exercise in this population resulting in mixed evidence regarding efficacy across functional domains. It is critical to investigate the methodological factors from the original interventions for a true understanding of these findings as to not outright dismiss exercise as beneficial. One example is Ohio’s replication of Reducing Disability in Alzheimer’s Disease (n=508), which resulted in no significant improvements in physical performance for individuals with dementia ((gait speed (p=.81), balance (p=.82), functional reach (p=.58)). In this investigation, along with many others, researchers were not guided by key principles of exercise science leading to critical intervention design and methodological flaws. Thus, exercise interventions for individuals with dementia need to include interpretations of non-findings and report key factors affecting the outcomes.


2018 ◽  
Vol 79 ◽  
pp. 223-234 ◽  
Author(s):  
Leili Jalili-Baleh ◽  
Hamid Nadri ◽  
Hamid Forootanfar ◽  
Alireza Samzadeh-Kermani ◽  
Tuba Tüylü Küçükkılınç ◽  
...  

Neurology ◽  
2003 ◽  
Vol 61 (1) ◽  
pp. 7-8 ◽  
Author(s):  
P. M. Mathews ◽  
R. A. Nixon

Author(s):  
Ashok K. Datusalia ◽  
Gurpreet Singh ◽  
Nikita Yadav ◽  
Sachin Gaun ◽  
Moumita Manik ◽  
...  

: Alzheimer’s disease (AD) is one of the most common neurodegenerative disease, which affect millions of people worldwide. Accumulation of amyloid-β plaques and hyperphosphorylated neurofibrillary tangles are the key mechanisms involved in the etiopathogenesis of AD, characterized by memory loss and behavioural changes. Effective therapies targeting AD pathogenesis are limited, making it the largest unmet clinical need. Unfortunately, the available drugs provide symptomatic relief and primary care, with no substantial impact on the disease pathology. However, in recent years researchers are working hard on several potential therapeutic targets to combat disease pathogenesis and few drugs have also reached clinical trials. In addition, drugs are being repurposed both in the preclinical and clinical studies for the treatment of AD. For instance, montelukast is most commonly used leukotriene receptor antagonist, for treating asthma and seasonal allergy. Its leukotriene antagonistic action can also be beneficial for the reduction of detrimental effects of leukotriene against neuro-inflammation, an hallmark feature of AD. The available marketed formulations of montelukast present challenges such as poor bioavailability and reduced uptake, reflecting the lack of effectiveness of its desired action in the CNS. While on the other side targeted drug delivery is a satisfactory approach to surpass the challenges associated with the therapeutic agents. This review will discuss the enhancement of montelukast treatment efficacy and its access to CNS, by using new approaches like nano-formulation, nasal gel, solid lipid formulation, nano-structure lipid carrier (NSLC), highlighting lessons learned to target AD pathologies and hurdles that persist.


2014 ◽  
Vol 5 (3) ◽  
Author(s):  
Yash Joshi ◽  
Domenico Praticò

AbstractAside from the well-known amyloid beta and tau pathologies found in Alzheimer’s disease (AD), neuroinflammation is a well-established aspect described in humans and animal models of the disease. Inflammatory perturbations are evident not only in neurons, but also in non-neuronal cells and cytokines in the AD brain. Although the amyloid hypothesis implicates amyloid beta (Aβ) as the prime initiator of the AD, brain inflammation in AD has a complex relationship between Aβ and tau. Using our work with the 5-lipoxygenase protein as an example, we suggest that at least in the case of AD, there is an interdependent and not necessarily hierarchical pathological relationship between Aβ, tau and inflammation.


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