The phrase "accelerated memory" is correct and usable in written English.
It can be used in contexts related to technology, neuroscience, or education, where speed or efficiency of memory processing is being discussed.
Example: "The new software utilizes accelerated memory techniques to enhance data retrieval speeds."
Alternatives: "enhanced memory" or "speeded-up memory".
Just as some will be stunned by the speed of sudoku champions, others will be astonished at the mental ingenuity of those who can work out that the answer to "Heggs (11)" is "exasperated" (eggs-haspirated).A study of 488 elderly people in the Bronx* found that taking part in crossword puzzles delayed the onset of accelerated memory decline by 2.54 years.
These results indicate that a positive regulatory loop involving IFN-γ and IL-18 signaling contributes to the accelerated memory CD8+ T cell proliferation during a recall response to antigen presented by DCs.
Also, 7-month-old 3xTg-AD mice with normal food intake exhibited the same memory impairment; their memory impairment was not as severe as that of 3xTg-AD mice with vitamin B6-deficient food, which indicated that vitamin B6-deficient food accelerated memory impairment (data not shown here).
As for the class II HDACs, it was shown that loss of HDAC5 accelerated memory decline in APPPS1-21 mice (Agis-Balboa et al, 2013).
The effect of education in crystalized intelligence is very well known; 26 on the clinical field, lack of education is considered a risk factor for accelerated memory decline, on the contrary education is considered a protective factor for cognitive impairment and dementia.
We posit that CCL2 facilitates Aβ oligomer formation in microglia and propose that such events accelerate memory dysfunction by affecting Aβ seeding in the brain.
Diabetes accelerates memory dysfunction in a continuous, slowly pathological process.
Considerable evidence shows that diabetes accelerates memory dysfunction in a continuous, slowly pathological process.
Indeed accelerating memory decline was seen to be greater in non-demented individuals with specific genetic risk for dementia (TOMM40 L and APOE e4) (Caselli et al. 2012).
This is consistent with a recent report that rapamycin treatment during T-cell contraction does not alter the number of CD8 T cells, but rather accelerates memory differentiation and produces T cells with phenotypic characteristics of highly functioning memory cells (Araki et al, 2009).
In conclusion, this study showed that chronic cerebral hypoperfusion accelerated reference memory impairment and hippocampal neuronal loss together with reduced Aβ deposition and cored plaque formation but an increased amount of filter-trap Aβ in the extracellular-enriched soluble brain fraction in APPSw/Ind mice.
