scholarly journals Progression of mild Alzheimer’s disease: knowledge and prediction models required for future treatment strategies

2013 ◽  
Vol 5 (5) ◽  
pp. 44 ◽  
Author(s):  
Carina Wattmo ◽  
Åsa K Wallin ◽  
Lennart Minthon
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prediction Models ◽  
Treatment Strategies ◽  
Disease Knowledge ◽  
Future Treatment

Medical Therapeutics Derived from Leeches (Phy. Annelida; Cl. Hirudinea)

2016 ◽  
Vol 3 (1) ◽  
Author(s):  
Christopher Everett Warren Clarke
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Heart Attack ◽  
Blood Feeding ◽  
Vascular Trauma ◽  
Biological Molecules ◽  
Future Treatment ◽  
Medical Therapeutics

Of all blood feeding invertebrates, few are more notorious than leeches. Throughout their existence as ectoparasites, leeches have evolved to release biological molecules in their saliva that act to counter the responses of the prey’s body to vascular trauma. Inadvertently, these very molecules have been used by humans for centuries for medicinal purposes; however, it is only recently that their cellular action has been elucidated. As a result, these compounds have been isolated and mass produced to treat a wide variety of conditions ranging from heart attack to Alzheimer’s disease and continued work suggests that these isolates will be an important future treatment for metastasis.

NF-κB as a Key Mediator of Brain Inflammation in Alzheimer’s Disease

2019 ◽  
Vol 18 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Chul Ju Hwang ◽  
Dong-Young Choi ◽  
Mi Hee Park ◽  
Jin Tae Hong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Treatment Strategies ◽  
Close Correlation ◽  
Specific Protein ◽  
Brain Inflammation ◽  
Cytokines And Chemokines ◽  
Inflammatory Drugs ◽  
Peptide Fibrils

Alzheimer’s disease is the most common form of dementia. It is characterized by betaamyloid peptide fibrils which are extracellular deposition of a specific protein, accompanied by extensive neuroinflammation. Various studies show the presence of a number of inflammation markers in the AD brain: elevated inflammatory cytokines and chemokines, and an accumulation of activated microglia in the damaged regions. NF-κB is a family of redox sensitive transcriptional factors, and it is known that NF-κB has binding sites in the promoter region of the genes involved in amyloidogenesis and inflammation. Long-term use of non-steroidal anti-inflammatory drugs prevents progression of AD and delays its onset, suggesting that there is a close correlation between NF-κB and AD pathogenesis. This study aims to (1) assess the association between NF-κB activity and AD through discussion of a variety of experimental and clinical studies on AD and (2) review treatment strategies designed to treat or prevent AD with NF-κB inhibitors.

scholarly journals Quantitative Longitudinal Predictions of Alzheimer’s Disease by Multi-Modal Predictive Learning

2021 ◽  
Vol 79 (4) ◽  
pp. 1533-1546
Author(s):  
Mithilesh Prakash ◽  
Mahmoud Abdelaziz ◽  
Linda Zhang ◽  
Bryan A. Strange ◽  
Jussi Tohka ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prediction Models ◽  
Predictive Performance ◽  
Absolute Error ◽  
Disease Stage ◽  
Disease Assessment ◽  
Disease Category ◽  
Modal Data ◽  
Predictive Learning

Background: Quantitatively predicting the progression of Alzheimer’s disease (AD) in an individual on a continuous scale, such as the Alzheimer’s Disease Assessment Scale-cognitive (ADAS-cog) scores, is informative for a personalized approach as opposed to qualitatively classifying the individual into a broad disease category. Objective: To evaluate the hypothesis that the multi-modal data and predictive learning models can be employed for future predicting ADAS-cog scores. Methods: Unimodal and multi-modal regression models were trained on baseline data comprised of demographics, neuroimaging, and cerebrospinal fluid based markers, and genetic factors to predict future ADAS-cog scores for 12, 24, and 36 months. We subjected the prediction models to repeated cross-validation and assessed the resulting mean absolute error (MAE) and cross-validated correlation (ρ) of the model. Results: Prediction models trained on multi-modal data outperformed the models trained on single modal data in predicting future ADAS-cog scores (MAE12, 24 & 36 months= 4.1, 4.5, and 5.0, ρ12, 24 & 36 months= 0.88, 0.82, and 0.75). Including baseline ADAS-cog scores to prediction models improved predictive performance (MAE12, 24 & 36 months= 3.5, 3.7, and 4.6, ρ12, 24 & 36 months= 0.89, 0.87, and 0.80). Conclusion: Future ADAS-cog scores were predicted which could aid clinicians in identifying those at greater risk of decline and apply interventions at an earlier disease stage and inform likely future disease progression in individuals enrolled in AD clinical trials.

scholarly journals Treatment strategies in Alzheimer’s disease: a review with focus on selenium supplementation

BioMetals ◽  
2016 ◽  
Vol 29 (5) ◽  
pp. 827-839 ◽  
Author(s):  
Jan Aaseth ◽  
Jan Alexander ◽  
Geir Bjørklund ◽  
Knut Hestad ◽  
Petr Dusek ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Treatment Strategies ◽  
Selenium Supplementation

scholarly journals Pharmacotherapy for Alzheimer’s disease: a perspective on treatment strategies in Japan

2018 ◽  
Vol 19 (12) ◽  
pp. 1301-1303
Author(s):  
Tomoyuki Nagata ◽  
Shinichiro Nakajima ◽  
Shunichiro Shinagawa ◽  
Yoshihiro Noda ◽  
Masaru Mimura
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Treatment Strategies

What Is the Rationale for New Treatment Strategies in Alzheimer's Disease?

CNS Spectrums ◽  
2004 ◽  
Vol 9 (S5) ◽  
pp. 6-12, 31 ◽  
Author(s):  
Michael A. Rogawski
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Behavioral Activation ◽  
Treatment Strategies ◽  
Amyloid Β ◽  
Functional Improvement ◽  
Amyloid Β Peptide ◽  
Global Functioning ◽  
Brain Functions ◽  
Che Inhibitors

AbstractAlzheimer's disease (AD) is characterized by the abnormal extracellular accumulation of amyloid β-peptide (Aβ) into neuritic plaques and the intraneuronal aggregation of the microtubule-associated protein tau to form neurofibrillary tangles. These molecular events are implicated in the selective damage to neural systems critical for the brain functions that are impaired in AD. Impairment of cholinergic neurotransmission may be an important factor underlying the defects in cognition and memory that characterize AD. Cholinesterase (ChE) inhibitors, such as donepezil, rivastigmine, and galantamine, cause symptomatic improvement by inhibiting the breakdown of the neurotransmitter acetylcholine to increase its synaptic availability and, in the case of galantamine, by also allosterically potentiating nicotinic cholinergic receptors. Other agents, including vitamin E, monoamine oxidase inhibitors, and statins, have shown some benefit in epidemiological studies and clinical trials although compelling evidence of their efficacy is lacking. Memantine, shown to cause cognitive and functional improvement, is not an ChE inhibitor and does not interact with marketed ChE inhibitors. While the mechanism of action of memantine in AD is not known, the principal pharmacologic actions at therapeutic dose are inhibition of ionotropic neurotransmitter receptors, specifically N-methyl-D-aspartate (NMDA), 5-HT3, and nicotinic receptors. Like other NMDA antagonists, memantine causes behavioral activation associated with enhanced cerebral glucose utilization. Studies have shown that memantine can reverse the decreased metabolic activity associated with AD, possibly accounting for its beneficial effects on cognition and global functioning. Memantine also has neuroprotective properties and can inhibit Aβ-induced neurodegeneration.

scholarly journals Feasibility of an Alzheimer's disease knowledge intervention in the Latino community

2018 ◽  
Vol 25 (5) ◽  
pp. 747-758 ◽  
Author(s):  
Jaime Perales ◽  
W. Todd Moore ◽  
Cielo Fernandez ◽  
Daniel Chavez ◽  
Mariana Ramirez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Knowledge ◽  
Latino Community
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