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Amyloid is formed through the polymerization of hundreds to thousands of monomeric peptides or proteins into long fibers. Amyloid formation involves a lag phase (also called nucleation phase), an exponential phase (also called growth phase) and a plateau phase (also called saturation phase), as shown in the figure.
Amyloid beta (Aβ, Abeta or beta-amyloid) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. [2] The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol ...
p3 peptide also known as amyloid β- peptide (Aβ) 17–40/42 is the peptide resulting from the α-and γ-secretase cleavage from the amyloid precursor protein ().It is known to be the major constituent of diffuse plaques observed in Alzheimer's disease (AD) brains and pre-amyloid plaques in people affected by Down syndrome.
The hippocampus is a structure in the brain that has been associated with various memory functions. It is part of the limbic system , and lies next to the medial temporal lobe. It is made up of two structures, the Ammon's Horn , and the Dentate gyrus , each containing different types of cells .
The normal function of Aβ is not certain, but plaques arise when the protein misfolds and begins to accumulate in the brain by a process of molecular templating ('seeding'). [36] Mathias Jucker and Lary Walker have likened this process to the formation and spread of prions in diseases known as spongiform encephalopathies or prion diseases.
Plots of the peptide amyloid-beta, which is thought to cause Alzheimer's disease, show the buildup of the peptide is within the DMN. [4] This prompted Randy Buckner and colleagues to propose the high metabolic rate from continuous activation of DMN causes more amyloid-beta peptide to accumulate in these DMN areas. [4]
The difference in memory between normal aging and a memory disorder is the amount of beta-amyloid deposits, hippocampal neurofibrillary tangles, or amyloid plaques in the cortex. If there is an increased amount, memory connections become blocked, memory functions decrease much more than what is normal for that age and a memory disorder is ...
This gave rise to the de novo protein synthesis theory: the formation of a long-term memory requires the synthesis of new proteins. Eric Kandel established many of the biochemical markers of learning and memory in the Aplysia (California sea slug) in the 1970s, as his findings suggested potential pathways surrounding protein synthesis. [2]