Application-Transparent Near-Memory Processing Architecture with Memory Channel Network

Author(s):  
Mohammad Alian ◽  
Seung Won Min ◽  
Hadi Asgharimoghaddam ◽  
Ashutosh Dhar ◽  
Dong Kai Wang ◽  
...  
IEEE Micro ◽  
1996 ◽  
Vol 16 (1) ◽  
pp. 12-18 ◽  
Author(s):  
R.B. Gillett

IEEE Micro ◽  
1997 ◽  
Vol 17 (1) ◽  
pp. 19-25 ◽  
Author(s):  
R. Gillett ◽  
R. Kaufmann

2021 ◽  
pp. 1-13
Author(s):  
Umesh M. Venkatesan ◽  
Amanda R. Rabinowitz ◽  
Stephanie J. Wolfert ◽  
Frank G. Hillary

BACKGROUND: Disrupted memory circuitry may contribute to post-traumatic amnesia (PTA) after traumatic brain injury (TBI). It is unclear whether duration of PTA (doPTA) uniquely impacts memory functioning in the chronic post-injury stage. OBJECTIVE: To examine the relationship between doPTA and memory functioning, independent of other cognitive abilities, in chronic moderate-to-severe TBI. METHODS: Participants were 82 individuals (median chronicity = 10.5 years) with available doPTA estimates and neuropsychological data. Composite memory, processing speed (PS), and executive functioning (EF) performance scores, as well as data on subjective memory (SM) beliefs, were extracted. DoPTA-memory associations were evaluated via linear modeling of doPTA with memory performance and clinical memory status (impaired/unimpaired), controlling for PS, EF and demographic covariates. Interrelationships between doPTA, objective memory functioning, and SM were assessed. RESULTS: DoPTA was significantly related to memory performance, even after covariate adjustment. Impairment in memory, but not PS or EF, was associated with a history of longer doPTA. SM was associated with memory performance, but unrelated to doPTA. CONCLUSIONS: Findings suggest a specific association between doPTA—an acute injury phenomenon—and chronic memory deficits after TBI. Prospective studies are needed to understand how underlying mechanisms of PTA shape distinct outcome trajectories, particularly functional abilities related to memory processing.


Author(s):  
Santiago A. Merlo ◽  
Maria J. Santos ◽  
Maria E. Pedreira ◽  
Emiliano Merlo

AbstractFully consolidated associative memories may be altered by alternative retrieval dependent memory processes. While a brief exposure to the conditioned stimulus (CS) can trigger reconsolidation of the original memory, a prolonged CS exposure will trigger memory extinction. The conditioned response is maintained after reconsolidation, but is inhibited after extinction, presumably by the formation of a new inhibitory memory trace. In rats and humans, it has been shown that CS exposure of intermediate duration leave the memory in an insensitive or limbo state. Limbo is characterised by the absence of reconsolidation or extinction. Here we investigated the evolutionary conserved nature of limbo using a contextual Pavlovian conditioning (CPC) memory paradigm in the crab Neohelice granulata. In animals with fully consolidated CPC memory, systemic administration of the protein synthesis inhibitor cycloheximide after 1 CS presentation disrupted the memory, presumably by interfering with memory reconsolidation. The same intervention given after 320 CSs prevented CPC memory extinction. Cycloheximide had no behavioural effect when administered after 80 CS presentations, a protocol that failed to extinguish CPC memory. Also, we observed that a stronger CPC memory engaged reconsolidation after 80 CS instead of limbo, indicating that memory strength affects the parametrical conditions to engage either reconsolidation or limbo. Altogether, these results indicate that limbo is an evolutionary conserved memory process segregating reconsolidation from extinction in the number of CSs space. Limbo appears as an intrinsic component of retrieval dependent memory processing, with a key function in the transition from memory maintenance to inhibition.Author statement (CRediT Roles)Santiago A. Merlo: Conceptualization, Data curation, Formal Analysis, Investigation, Software, Validation, Visualization, Writing – original draft, Writing – review & editing.Jimena Santos: Investigation, Writing – review & editing.Maria Eugenia Pedreira: Conceptualization, Funding acquisition, Project administration, Resources, Supervision, Validation, Writing – original draft, Writing – review & editing.Emiliano Merlo: Conceptualization, Funding acquisition, Project administration, Resources, Supervision, Validation, Writing – original draft, Writing – review & editing.


2020 ◽  
Vol 21 (18) ◽  
pp. 6918
Author(s):  
Samantha D. Creighton ◽  
Gilda Stefanelli ◽  
Anas Reda ◽  
Iva B. Zovkic

The neuronal epigenome is highly sensitive to external events and its function is vital for producing stable behavioral outcomes, such as the formation of long-lasting memories. The importance of epigenetic regulation in memory is now well established and growing evidence points to altered epigenome function in the aging brain as a contributing factor to age-related memory decline. In this review, we first summarize the typical role of epigenetic factors in memory processing in a healthy young brain, then discuss the aspects of this system that are altered with aging. There is general agreement that many epigenetic marks are modified with aging, but there are still substantial inconsistencies in the precise nature of these changes and their link with memory decline. Here, we discuss the potential source of age-related changes in the epigenome and their implications for therapeutic intervention in age-related cognitive decline.


Author(s):  
Jörg-Tobias Kuhn ◽  
Elena Ise ◽  
Julia Raddatz ◽  
Christin Schwenk ◽  
Christian Dobel

Abstract. Objective: Deficits in basic numerical skills, calculation, and working memory have been found in children with developmental dyscalculia (DD) as well as children with attention-deficit/hyperactivity disorder (ADHD). This paper investigates cognitive profiles of children with DD and/or ADHD symptoms (AS) in a double dissociation design to obtain a better understanding of the comorbidity of DD and ADHD. Method: Children with DD-only (N = 33), AS-only (N = 16), comorbid DD+AS (N = 20), and typically developing controls (TD, N = 40) were assessed on measures of basic numerical processing, calculation, working memory, processing speed, and neurocognitive measures of attention. Results: Children with DD (DD, DD+AS) showed deficits in all basic numerical skills, calculation, working memory, and sustained attention. Children with AS (AS, DD+AS) displayed more selective difficulties in dot enumeration, subtraction, verbal working memory, and processing speed. Also, they generally performed more poorly in neurocognitive measures of attention, especially alertness. Children with DD+AS mostly showed an additive combination of the deficits associated with DD-only and A_Sonly, except for subtraction tasks, in which they were less impaired than expected. Conclusions: DD and AS appear to be related to largely distinct patterns of cognitive deficits, which are present in combination in children with DD+AS.



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