More data-driven processing at retrieval reduces age-related memory deficits.

2010 ◽  
Vol 64 (2) ◽  
pp. 117-123
Author(s):  
Lucie Angel ◽  
Séverine Fay ◽  
Badiâa Bouazzaoui ◽  
Michel Isingrini
Keyword(s):  
Memory Deficits ◽  
Data Driven ◽  
Age Related

scholarly journals Chondroitin 6-sulphate is required for neuroplasticity and memory in ageing

2021 ◽  
Author(s):  
Sujeong Yang ◽  
Sylvain Gigout ◽  
Angelo Molinaro ◽  
Yuko Naito-Matsui ◽  
Sam Hilton ◽  
...  
Keyword(s):  
Chondroitin Sulphate ◽  
Memory Loss ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Aged Mice ◽  
Age Related ◽  
Term Potentiation ◽  
Early Memory

AbstractPerineuronal nets (PNNs) are chondroitin sulphate proteoglycan-containing structures on the neuronal surface that have been implicated in the control of neuroplasticity and memory. Age-related reduction of chondroitin 6-sulphates (C6S) leads to PNNs becoming more inhibitory. Here, we investigated whether manipulation of the chondroitin sulphate (CS) composition of the PNNs could restore neuroplasticity and alleviate memory deficits in aged mice. We first confirmed that aged mice (20-months) showed memory and plasticity deficits. They were able to retain or regain their cognitive ability when CSs were digested or PNNs were attenuated. We then explored the role of C6S in memory and neuroplasticity. Transgenic deletion of chondroitin 6-sulfotransferase (chst3) led to a reduction of permissive C6S, simulating aged brains. These animals showed very early memory loss at 11 weeks old. Importantly, restoring C6S levels in aged animals rescued the memory deficits and restored cortical long-term potentiation, suggesting a strategy to improve age-related memory impairment.

scholarly journals Individual variation in brain microstructural-cognition relationships in aging

2021 ◽  
Author(s):  
Raihaan Patel ◽  
Clare E. Mackay ◽  
Michelle G. Jansen ◽  
Gabriel A. Devenyi ◽  
M. Clare O’Donoghue ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Performance ◽  
Late Life ◽  
Older Age ◽  
Data Driven ◽  
Semantic Fluency ◽  
Cognitive Domains ◽  
Age Related ◽  
Brain Microstructure ◽  
Age Related Cognitive Decline

AbstractWhile all individuals are susceptible to age-related cognitive decline, significant inter- and intra-individual variability exists. However, the sources of this variation remain poorly understood. Here, we examined the association between 30-year trajectories of cognitive decline and multimodal indices of brain microstructure and morphology in older age. We used the Whitehall II Study, an extensively characterised cohort using 3T brain magnetic resonance images acquired at older age (mean age = 69.52 ± 4.9) and 5 repeated cognitive performance assessments between mid-life (mean age = 53.2 ± 4.9 years) and late-life (mean age = 67.7 ± 4.9). Using non-negative matrix factorization, we identified 10 brain microstructural components that integrate measures of cortical thickness, surface area, fractional anisotropy, and mean and radial diffusivities. We observed two modes of variance that describe the association between cognition and brain microstructure. The first describes variations in 5 microstructural components associated with low mid-life performance across multiple cognitive domains, decline in reasoning abilities, but a relative maintenance of lexical and semantic fluency from mid-to-late life. The second describes variations in 5 microstructural components that are associated with low mid-life performance in lexical fluency, semantic fluency and short-term memory performance, but a retention of abilities in multiple domains from mid-to-late life. The extent to which a subject loads onto a latent variables predicts their future cognitive performance 3.2 years later (mean age = 70.87 ± 4.9). This data-driven approach highlights a complex pattern of brain-behavior relationships, wherein the same individuals express both decline and maintenance in function across cognitive domains and in brain structural features.Significance StatementAlthough declines in cognitive performance are an established aspect of aging, inter- and intra-individual variation exists. Nevertheless, the sources of this variation remain unclear. We analyse a unique sample to examine associations between 30-year trajectories of cognitive decline and multimodal indices of brain anatomy in older age. Using data-driven techniques, we find that age-related cognitive decline is not uniform. Instead, each individual expresses a mixture of maintenance and decline across cognitive domains, that are associated with a mixture of preservation and degeneration of brain structure. Further, we find the primary determinants of late-life cognitive performance are mid-life performance and higher brain surface area. These results suggest that early and mid-life preventative measures may be needed to reduce age-related cognitive decline.

Does Declining Mitochondrial NAD+ and Unscheduled Opening of Mitochondrial Transition Pore Promote Mammalian Aging?

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. SCI-3-SCI-3
Author(s):  
David Sinclair ◽  
Angela V. Hafner ◽  
Ana Gomes ◽  
Jing Liang ◽  
Yana Cen ◽  
...  
Keyword(s):  
Board Of Directors ◽  
Memory Deficits ◽  
Dependent Manner ◽  
Advisory Committees ◽  
Model Of Alzheimer’S Disease ◽  
Age Related ◽  
Promote Cell Survival ◽  
Mitochondrial Defects ◽  
Equity Ownership ◽  
Mitochondrial Transition Pore

Abstract Abstract SCI-3 The processes that lead to the susceptibility of post-mitotic tissues to diseases of aging are poorly understood, but mitochondria are considered a key regulator. SIRT3 is mitochondrial sirtuin, a member a family of NAD+-dependent deacetylases. We have previously shown that increased levels of NAD+ in mitochondria promote cell survival in a SIRT3-dependent manner, but how this protection is mediated is unknown. Here we show that mitochondrial NAD+ levels decline dramatically with age and that SIRT3 is a critical component and regulator of the mitochondrial transition pore (MTP). Mice lacking SIRT3 exhibit hyperacetylation of the MTP with age, and as a result, develop multiple defects in post-mitotic tissues as they age, including mitochondrial defects, susceptibility to cardiac failure, and learning and memory deficits. In a mouse model of Alzheimer's disease (AD), SIRT3 knockout mice show striking phenotypes including small size, kyphosis, and a markedly reduced lifespan. Similar to mice, human brain samples show that acetylation of the MTP increases with age and with AD. These findings indicate that declining NAD levels with age lead to memory deficits and accelerate age-related diseases in post-mitotic tissues due to a decline in SIRT3 activity and unscheduled opening of the MTP. Disclosures: Sinclair: GlaxoSmithKline: Consultancy, Equity Ownership, Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.

scholarly journals Changes in pattern completion – A key mechanism to explain age-related recognition memory deficits?

Cortex ◽  
2015 ◽  
Vol 64 ◽  
pp. 343-351 ◽  
Author(s):  
Paula Vieweg ◽  
Matthias Stangl ◽  
Lorelei R. Howard ◽  
Thomas Wolbers
Keyword(s):  
Recognition Memory ◽  
Memory Deficits ◽  
Pattern Completion ◽  
Age Related

Tetrahydroaminoacridine alleviates medial septal lesion-induced and age-related spatial reference but not working memory deficits

1991 ◽  
Vol 49 (6) ◽  
pp. 1147-1152 ◽  
Author(s):  
Paavo Riekkinen ◽  
Minna Aaltonen ◽  
Jouni Sirviö ◽  
Paavo Riekkinen
Keyword(s):  
Working Memory ◽  
Septal Lesion ◽  
Memory Deficits ◽  
Spatial Reference ◽  
Age Related

scholarly journals Relationships between default-mode network connectivity, medial temporal lobe structure, and age-related memory deficits

2015 ◽  
Vol 36 (1) ◽  
pp. 265-272 ◽  
Author(s):  
Andrew M. Ward ◽  
Elizabeth C. Mormino ◽  
Willem Huijbers ◽  
Aaron P. Schultz ◽  
Trey Hedden ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Default Mode Network ◽  
Medial Temporal Lobe ◽  
Network Connectivity ◽  
Memory Deficits ◽  
Default Mode ◽  
Age Related

Biological Markers of Age-Related Memory Deficits

CNS Drugs ◽  
2006 ◽  
Vol 20 (2) ◽  
pp. 153-166 ◽  
Author(s):  
Thomas C Foster
Keyword(s):  
Biological Markers ◽  
Memory Deficits ◽  
Age Related

scholarly journals CREB overexpression in dorsal CA1 ameliorates long-term memory deficits in aged rats

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Xiao-Wen Yu ◽  
Daniel M Curlik ◽  
M Matthew Oh ◽  
Jerry CP Yin ◽  
John F Disterhoft
Keyword(s):  
Molecular Mechanisms ◽  
Pyramidal Neurons ◽  
Dorsal Hippocampus ◽  
Memory Deficits ◽  
Camp Response Element Binding ◽  
Intrinsic Excitability ◽  
Long Term Memory ◽  
Term Memory ◽  
Age Related

The molecular mechanisms underlying age-related cognitive deficits are not yet fully elucidated. In aged animals, a decrease in the intrinsic excitability of CA1 pyramidal neurons is believed to contribute to age-related cognitive impairments. Increasing activity of the transcription factor cAMP response element-binding protein (CREB) in young adult rodents facilitates cognition, and increases intrinsic excitability. However, it has yet to be tested if increasing CREB expression also ameliorates age-related behavioral and biophysical deficits. To test this hypothesis, we virally overexpressed CREB in CA1 of dorsal hippocampus. Rats received CREB or control virus, before undergoing water maze training. CREB overexpression in aged animals ameliorated the long-term memory deficits observed in control animals. Concurrently, cells overexpressing CREB in aged animals had reduced post-burst afterhyperpolarizations, indicative of increased intrinsic excitability. These results identify CREB modulation as a potential therapy to treat age-related cognitive decline.

scholarly journals Age-related memory deficits are associated with changes in protein degradation in brain regions critical for trace fear conditioning

2020 ◽  
Vol 91 ◽  
pp. 160-166 ◽  
Author(s):  
Brooke N. Dulka ◽  
Shane E. Pullins ◽  
Patrick K. Cullen ◽  
James R. Moyer ◽  
Fred J. Helmstetter
Keyword(s):  
Protein Degradation ◽  
Fear Conditioning ◽  
Memory Deficits ◽  
Brain Regions ◽  
Trace Fear Conditioning ◽  
Age Related ◽  
Trace Fear

scholarly journals Normalization of hippocampal retinoic acid level corrects age-related memory deficits in rats

2020 ◽  
Vol 85 ◽  
pp. 1-10 ◽  
Author(s):  
Fabien Dumetz ◽  
Corinne Buré ◽  
Serge Alfos ◽  
Marc Bonneu ◽  
Emmanuel Richard ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Acid Level ◽  
Memory Deficits ◽  
Age Related
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