Alzheimer's disease causes loss of memory and deterioration of mental abilities is utmost predominant neurodegenerative disease accounting 70-80% cases of dementia. The appearance of plaques of amyloid-β and neurofibrillary tangles in the brain post-mortems of Alzheimer's patients established them as key participants in the etiology of Alzheimer's disease. Exosomes exist as extracellular vesicles of nano-size which are present throughout the body. Exosomes are known to spread toxic hyperphosphorylated tau and amyloid-β between the cells and are linked to the loss of neurons by inducing apoptosis. Exosomes have progressed from cell trashcans to multifunctional organelles which are involved in various functions like internalisation and transmission of macromolecules such as lipids, proteins, and nucleic acids. This review covers current findings on relationship of exosomes in biogenesis and angiogenesis of Alzheimer's disease and functions of exosomes in the etiology of AD. Furthermore, the roles of exosomes in development, diagnosis, treatment, and its importance as therapeutic targets and biomarkers for Alzheimer's disease have also been highlighted.
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Functional classification of tauopathy strains reveals the role of protofilament core residues.
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Distinct tau amyloid assemblies underlie diverse tauopathies but defy rapid classification. Cell and animal experiments indicate tau functions as a prion, as different strains propagated in cells cause unique, transmissible neuropathology after inoculation. Strain amplification requires compatibility of the monomer and amyloid template.
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Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377 Munich, Germany.
In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. However, the pathophysiological link between Aβ and tau remains unclear, which hinders therapeutic efforts to attenuate Aβ-related tau accumulation. Aβ has been found to trigger neuronal hyperactivity and hyperconnectivity, and preclinical research has shown that tau spreads across connected neurons in an activity-dependent manner.
View Article and Find Full Text PDFDown syndrome, resulting from trisomy of human chromosome 21, is a common form of chromosomal disorder that results in intellectual disability and altered risk of several medical conditions. Individuals with Down syndrome have a greatly increased risk of Alzheimer's disease (DSAD), due to the presence of the APP gene on chromosome 21 that encodes the amyloid-β precursor protein (APP). APP can be processed to generate amyloid-β, which accumulates in plaques in the brains of people who have Alzheimer's disease and is the upstream trigger of disease.
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