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| http://dx.doi.org/10.1038/s41421-020-0147-1 | DOI Listing |
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Drug Development.
Alzheimers Dement
December 2024
Case Western Reserve University, Cleveland, OH, USA.
Background: Traumatic Brain Injury (TBI) is one of the most common nonheritable causes of Alzheimer's disease (AD). However, there is lack of effective treatment for both AD and TBI. We posit that network-based integration of multi-omics and endophenotype disease module coupled with large real-world patient data analysis of electronic health records (EHR) can help identify repurposable drug candidates for the treatment of TBI and AD.
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Alzheimers Dement
December 2024
Federal University of Technology, Akure, Ondo, Nigeria.
Background: In recent decades, epidemiological and experimental studies have looked into the role of pesticides, particularly the herbicide paraquat, in the development of Parkinson's disease. Horseradish tree (Moringa oleifera) is an ethnobotanical plant with lots of therapeutic potential, but there is a dearth of information on the bioactive properties of the seed alkaloid extracts.
Method: This study examined the modulatory effects of various concentrations of an alkaloid extract from the seeds of Horseradish Tree (Moringa oleifera) on the survival rate of flies exposed to paraquat, as well as certain biochemical and molecular markers related to Parkinson's disease in the heads of the flies.
Drug Development.
Alzheimers Dement
December 2024
UCSF Weill Institute for Neurosciences, San Francisco, CA, USA.
Background: Efforts to genetically reverse C9orf72 pathology have been hampered by our incomplete understanding of the regulation of this complex locus.
Method: We generated five different genomic excisions at the C9orf72 locus in a patient-derived iPSC line and a WT line (11 total isogenic lines), and examined gene expression and pathological hallmarks of C9 FTD/ALS in motor neurons differentiated from these lines. Comparing the excisions in these isogenic series removed the confounding effects of different genomic backgrounds and allowed us to probe the effects of specific genomic changes.
Background: Accumulating evidence suggests that the presynaptic protein α-synuclein (α-syn), is involved in the pathophysiology of AD and elevated in the cerebrospinal fluid (CSF). The role of Natural Killer (NK) cells of the innate immune system in AD has largely been overlooked. In a murine model, depletion of NK cells augmented the accumulation of pathological α-syn.
View Article and Find Full Text PDFDrug Development.
Alzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA.
Background: Apolipoprotein E4 (apoE4) has been identified as the major genetic risk factor for late onset Alzheimer's disease (AD). Our lab has demonstrated that chronic administration of Aβ12-28P, a synthetic peptide that blocks apoE4/Aβ binding, in middle-aged transgenic AD mice significantly ameliorates pathology progression, resulting in reduced Aβ plaques deposition and cerebral amyloid angiopathy (CAA) along with improved memory and cognition. However, whether blocking apoE4/Aβ interaction by Aβ12-28P also has an ameliorating effect on the neuronal and cognitive function of old AD mice where Aβ pathology has been extensively developed remains unknown.
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