Sentences with phrase «extracellular brain plaques»

Not exact matches

Exhaustive brain research has pieced together how extracellular beta - amyloid plaques and intracellular neurofibrillary tangles of tau proteins are strongly linked to the neurodegenerative pathology of Alzheimer's disease.

One 2013 study showed that the extracellular space in a mouse's brain expands by 60 percent during sleep, and clearance of amyloid plaque (one protein implicated in Alzheimer's) spikes.

Furthermore, in brains from APP transgenic mice conformation - specific antibodies have revealed the early appearance of intraneuronal fibrillar and oligomeric Aβ immunoreactivity, which declined as amyloid plaques appeared, and further became evident in the extracellular space [10].

Furthermore, the CSF detection of Aβ peptides suggest a dynamic state of these molecules, where some accumulate inside neurons, and some are exported to the extracellular space, from where they can reach the CSF even in the absence of amyloid plaques in the brain parenchyma.

These plaques are extracellular aggregations of a small protein called beta - amyloid that are prominent in diseased patients» brains, as well as in mouse models of the disease.

''... we hypothesize that repeated stress - related allostatic overload may affect brain function at three basic levels: (a) at the cellular level, it may compromise proteostasis (e.g. tau protein), organelles homeostasis, and induce epigenetic changes in neuronal DNA; (b) at the tissue level it may affect intracellular communication (synaptic contacts), number of cells (reduction of neuronal density), composition of the extracellular matrix (accumulation of amyloid plaques), and neuroinflammation; (c) at the systemic levels it may alter the brain's regulation of behavior (cognitive decline).

Glycation is a factor of glucose concentration exposure and time, with more AGEs forming upon longer exposure to higher concentrations of glucose.33 It follows that in a body that is hyperinsulinemic, and a brain that is insulin - resistant, the peripheral hyperinsulinism will inhibit the clearance of soluble Aβ by IDE, thereby causing it to remain in the extracellular space for an extended amount of time, and the functional «hyperglycemia» in the brain will provide an elevated level of glucose — the perfect storm for glycation of Aβ and its aggregation into insoluble plaques.

These include insoluble extracellular plaques made of beta - amyloid peptide (Aβ); intracellular neurofibrillary tangles (NFTs) resulting from the hyperphosphorylation of tau (a microtubule - associated protein); loss of hippocampal neurons; a decrease in production of brain acetylcholine; and a marked decline in glucose usage in regions of the brain associated with memory and learning.5,11,20 - 22 All of these changes can be logically explained as the sequelae resulting from long - term dysregulation of insulin signaling and glucose metabolism.