Nat Rev Immunol
December 2024
Background: Glycogen synthase-3 kinase (GSK3) is one of the major contributors of tau hyperphosphorylation linked to neurofibrillary tangles in Alzheimer's disease (AD).
Objective: To determine a mechanism of GSK-3β activation by two periodontal bacteria consistently confirmed in AD autopsied brains.
Methods: FDC381 and ATCC10301 conditioned media were collected.
Alzheimer's disease (AD) is a neurodegenerative disease and the most common example of dementia. The neuropathological features of AD are the abnormal deposition of extracellular amyloid-β (Aβ) and intraneuronal neurofibrillary tangles with hyperphosphorylated tau protein. It is recognized that AD starts in the frontal cerebral cortex, and then it progresses to the entorhinal cortex, the hippocampus, and the rest of the brain.
View Article and Find Full Text PDFBackground: Oral infection has been implicated in the possible etiology of Alzheimer's disease.
Objective: To detect amyloid-β (Aβ) within microbial biofilms.
Methods: Freshly extracted teeth ( = 87) with periodontal disease were separated into Group A ( = 11), with primary root canal infection and Group B ( = 21) with failed endodontic treatment identified by the presence of, gutta percha root filling.
Alzheimer's disease (AD) is a leading neurodegenerative disease with deteriorating cognition as its main clinical sign. In addition to the clinical history, it is characterized by the presence of two neuropathological hallmark lesions; amyloid-beta (Aβ) and neurofibrillary tangles (NFTs), identified in the brain at post-mortem in specific anatomical areas. Recently, it was discovered that NFTs occur initially in the subcortical nuclei, such as the locus coeruleus in the pons, and are said to spread from there to the cerebral cortices and the hippocampus.
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