scholarly journals Accelerated long‐term forgetting is a BACE1 inhibitor‐reversible incipient cognitive phenotype in Alzheimer’s disease model mice

2021 ◽  
Author(s):  
Masuo Ohno
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Model ◽  
Bace1 Inhibitor ◽  
Cognitive Phenotype

Long-term immunomodulatory effect of amniotic stem cells in an Alzheimer's disease model

2013 ◽  
Vol 34 (10) ◽  
pp. 2408-2420 ◽  
Author(s):  
Kyung-Sul Kim ◽  
Hyun Sook Kim ◽  
Ji-Min Park ◽  
Han Wool Kim ◽  
Mi-kyung Park ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Disease Model ◽  
Immunomodulatory Effect

scholarly journals Unexpected Early Proteomic Changes in Alzheimer’s Disease Model Mice Synaptosomes

2017 ◽  
Author(s):  
Kerri Ball ◽  
Addolorata Pisconti ◽  
Kelly Grounds ◽  
William M. Old ◽  
Michael H. B. Stowell
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Model ◽  
Long Term Potentiation ◽  
Label Free ◽  
Amyloid Accumulation ◽  
Term Potentiation ◽  
Novel Associations ◽  
Statistical Criteria

AbstractWe have employed label-free quantitative proteomics of wild-type and Alzheimer’s disease (AD) model mice synaptosomes to investigate proteomic changes occurring during AD progression as a prelude to analysis in humans. More than 4000 proteins were analyzed using multiple analysis tools and statistical criteria. Pathway enrichment identified numerous pathways consistent with the current AD knowledge base, including dysregulation of Glutamate Receptor Signaling, Synaptic Long Term Potentiation and Depression, Rho and Rac Signaling, Calcium Signaling, and Oxidative Phosphorylation and Mitochondrial Dysfunction. Additionally, the data demonstrate that a large number of changes occur in the proteome very early relative to the onset of both traditional disease markers such as amyloid accumulation, tau phosphorylation and cognitive dysfunction. These early changes include a number of dysregulated proteins that have novel associations with AD progression. These results reinforce the importance of mechanistic investigations in early disease progression long before the classical markers of Alzheimer’s disease are observed.

Integrated Biomarkers for Depression in Alzheimer’s Disease: A Critical Review

2017 ◽  
Vol 14 (4) ◽  
pp. 441-452 ◽  
Author(s):  
Sofia Wenzler ◽  
Christian Knochel ◽  
Ceylan Balaban ◽  
Dominik Kraft ◽  
Juliane Kopf ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Affect Regulation ◽  
Current Evidence ◽  
Diagnostic Process ◽  
Neuropsychiatric Manifestation ◽  
The Brain ◽  
Control Functional

Depression is a common neuropsychiatric manifestation among Alzheimer’s disease (AD) patients. It may compromise everyday activities and lead to a faster cognitive decline as well as worse quality of life. The identification of promising biomarkers may therefore help to timely initiate and improve the treatment of preclinical and clinical states of AD, and to improve the long-term functional outcome. In this narrative review, we report studies that investigated biomarkers for AD-related depression. Genetic findings state AD-related depression as a rather complex, multifactorial trait with relevant environmental and inherited contributors. However, one specific set of genes, the brain derived neurotrophic factor (BDNF), specifically the Val66Met polymorphism, may play a crucial role in AD-related depression. Regarding neuroimaging markers, the most promising findings reveal structural impairments in the cortico-subcortical networks that are related to affect regulation and reward / aversion control. Functional imaging studies reveal abnormalities in predominantly frontal and temporal regions. Furthermore, CSF based biomarkers are seen as potentially promising for the diagnostic process showing abnormalities in metabolic pathways that contribute to AD-related depression. However, there is a need for standardization of methodological issues and for replication of current evidence with larger cohorts and prospective studies.

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.

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