scholarly journals OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Ryan J Bevan ◽  
Pete A Williams ◽  
Caroline T Waters ◽  
Rebecca Thirgood ◽  
Amanda Mui ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Performance ◽  
Memory Deficits ◽  
Metabolic Dysfunction ◽  
Neuronal Function ◽  
Synaptic Density ◽  
Ca1 Neurons ◽  
Mitochondrial Homeostasis ◽  
Age Related ◽  
Spatial Novelty

Abstract A healthy mitochondrial network is essential for the maintenance of neuronal synaptic integrity. Mitochondrial and metabolic dysfunction contributes to the pathogenesis of many neurodegenerative diseases including dementia. OPA1 is the master regulator of mitochondrial fusion and fission and is likely to play an important role during neurodegenerative events. To explore this, we quantified hippocampal dendritic and synaptic integrity and the learning and memory performance of aged Opa1 haploinsufficient mice carrying the Opa1Q285X mutation (B6; C3-Opa1Q285STOP; Opa1+/−). We demonstrate that heterozygous loss of Opa1 results in premature age-related loss of spines in hippocampal pyramidal CA1 neurons and a reduction in synaptic density in the hippocampus. This loss is associated with subtle memory deficits in both spatial novelty and object recognition. We hypothesize that metabolic failure to maintain normal neuronal activity at the level of a single spine leads to premature age-related memory deficits. These results highlight the importance of mitochondrial homeostasis for maintenance of neuronal function during ageing.

scholarly journals The beneficial effects of berries on cognition, motor behaviour and neuronal function in ageing

2015 ◽  
Vol 114 (10) ◽  
pp. 1542-1549 ◽  
Author(s):  
Barbara Shukitt-Hale ◽  
Donna F. Bielinski ◽  
Francis C. Lau ◽  
Lauren M. Willis ◽  
Amanda N. Carey ◽  
...  
Keyword(s):  
Working Memory ◽  
Memory Performance ◽  
Hippocampal Neurogenesis ◽  
Fischer 344 Rats ◽  
Neuronal Function ◽  
Beneficial Effects ◽  
Fischer 344 ◽  
Age Related ◽  
Berry Fruits ◽  
Relative Differences

AbstractPreviously, it has been shown that strawberry (SB) or blueberry (BB) supplementations, when fed to rats from 19 to 21 months of age, reverse age-related decrements in motor and cognitive performance. We have postulated that these effects may be the result of a number of positive benefits of the berry polyphenols, including decreased stress signalling, increased neurogenesis, and increased signals involved in learning and memory. Thus, the present study was carried out to examine these mechanisms in aged animals by administering a control, 2 % SB- or 2 % BB-supplemented diet to aged Fischer 344 rats for 8 weeks to ascertain their effectiveness in reversing age-related deficits in behavioural and neuronal function. The results showed that rats consuming the berry diets exhibited enhanced motor performance and improved cognition, specifically working memory. In addition, the rats supplemented with BB and SB diets showed increased hippocampal neurogenesis and expression of insulin-like growth factor 1, although the improvements in working memory performance could not solely be explained by these increases. The diverse polyphenolics in these berry fruits may have additional mechanisms of action that could account for their relative differences in efficacy.

Age-related learning and memory deficits in odor-reward association in rats

1996 ◽  
Vol 17 (1) ◽  
pp. 31-40 ◽  
Author(s):  
F.S. Roman ◽  
B. Alescio-Lautier ◽  
B. Soumireu-Mourat
Keyword(s):  
Learning And Memory ◽  
Memory Deficits ◽  
Age Related ◽  
Learning And Memory Deficits

scholarly journals Learning and Memory in the Aging Brain: The Function of Declarative and Nondeclarative Memory Over the Life Span

2018 ◽  
Author(s):  
Nichole Lighthall ◽  
Lindsay Conner ◽  
Kelly Sullivan Giovanello
Keyword(s):  
Learning And Memory ◽  
Age Differences ◽  
Memory Performance ◽  
Human Memory ◽  
Memory Systems ◽  
Aging Brain ◽  
Aging Research ◽  
Age Related ◽  
Neural Underpinnings

Human memory consists of distinct learning and memory systems, each contributing in unique ways to the acquisition, retention, and subsequent retrieval of information. This chapter focuses on age-related changes to long-term declarative (episodic and semantic memory) and nondeclarative (priming, classical conditioning, procedural and reinforcement learning) systems. Although these systems exhibit considerable independence in processing characteristics and neural underpinnings, accumulating evidence points to interactions between systems, which may increase observable age differences in learning and memory performance. Thus, while this chapter largely highlights age effects within traditional memory-system boundaries, a frontier in aging research is emerging at their intersections.

scholarly journals AMPK Modulates Associative Learning via Neuronal Mitochondrial Fusion in C. elegans

2020 ◽  
Author(s):  
Caroline C. Escoubas ◽  
Vanessa Laversenne ◽  
Emina Tabakovic ◽  
Heather J. Weir ◽  
Nicole Clark ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Associative Learning ◽  
Therapeutic Option ◽  
Mitochondrial Fusion ◽  
Ampk Activation ◽  
Neuronal Function ◽  
Learning Capacity ◽  
C Elegans ◽  
Mitochondrial Homeostasis ◽  
Age Related

ABSTRACTLoss of metabolic homeostasis is one of the hallmarks of the aging process that might contribute to pathogenesis by creating a permissive landscape over which neurodegenerative diseases can take hold. AMPK, a conserved energy sensor, extends lifespan and is protective in some neurodegenerative models. AMPK regulates mitochondrial homeostasis and morphology, however, whether mitochondrial regulation causally links AMPK to protection against loss of neuronal function with aging and diseases remains unclear. Here we use an associative learning protocol in C. elegans as a readout of neuronal function and show that AMPK activation enhances associative learning and prevents age-related loss of learning capacity. AMPK promotes neuronal mitochondrial fusion and mitochondrial fragmentation via fzo-1 deletion blocks AMPK’s effects on associative learning. Restoring mitochondrial fusion capacity specifically in the neurons rescued learning capacity downstream of AMPK. Finally, AMPK activation rescues neuronal Aβ1-42 induced loss of associative learning. Overall, our results suggest that targeting neuronal metabolic flexibility may be a viable therapeutic option to restore neuronal function in the context of aging and neurodegenerative diseases.

Methylphenidate treatment increases hippocampal BDNF levels but does not improve memory deficits in hypoxic-ischemic rats

2020 ◽  
Vol 34 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Patrícia Maidana Miguel ◽  
Bruna Ferrary Deniz ◽  
Heloísa Deola Confortim ◽  
Wellington de Almeida ◽  
Loise Peres Bronauth ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Performance ◽  
Memory Deficits ◽  
The Novel ◽  
Dose Response Relationship ◽  
Stimulant Drug ◽  
Attentional Deficits ◽  
Hyperactivity Disorder ◽  
Male Wistar Rats ◽  
Learning And Memory Deficits

Background: Methylphenidate (MPH) is a stimulant drug mainly prescribed to treat cognitive impairments in attention-deficit/hyperactivity disorder (ADHD). We demonstrated that neonatal hypoxia-ischemia (HI) induced attentional deficits in rats and MPH administration reversed these deficits. However, MPH effects on memory deficits after the HI procedure have not been evaluated yet. Aims: We aimed to analyze learning and memory performance of young hypoxic-ischemic rats after MPH administration and associate their performance with brain-derived neurotrophic factor (BDNF) levels in the prefrontal cortex and hippocampus. Methods: Male Wistar rats were divided into four groups ( n=11–13/group): control saline (CTS), control MPH (CTMPH), HI saline (HIS) and HIMPH. The HI procedure was conducted at post-natal day (PND) 7 and memory tasks between PND 30 and 45. MPH administration (2.5 mg/kg, i.p.) occurred 30 min prior to each behavioral session and daily, for 15 days, for the BDNF assay ( n=5–7/group). Results: As expected, hypoxic-ischemic animals demonstrated learning and memory deficits in the novel-object recognition (NOR) and Morris water maze (MWM) tasks. However, MPH treatment did not improve learning and memory deficits of these animals in the MWM—and even disrupted the animals’ performance in the NOR task. Increased BDNF levels were found in the hippocampus of HIMPH animals, which seem to have been insufficient to improve memory deficits observed in this group. Conclusions: The MPH treatment was not able to improve memory deficits resulting from the HI procedure considering a dose of 2.5 mg/kg. Further studies investigating different MPH doses would be necessary to determine a dose–response relationship in this model.

Age-related changes in learning and memory and cholinergic neuronal function in senescence accelerated mice (SAM)

1995 ◽  
Vol 72 (1-2) ◽  
pp. 49-55 ◽  
Author(s):  
Atsumi Nitta ◽  
Kazumasa Naruhashi ◽  
Masayuki Umemura ◽  
Takaaki Hasegawa ◽  
Shoei Furukawa ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Neuronal Function ◽  
Age Related ◽  
Senescence Accelerated Mice ◽  
Age Related Changes

scholarly journals Memory Deficits Precede Increases in Depressive Symptoms in Later Adulthood

2018 ◽  
Vol 74 (6) ◽  
pp. 943-953 ◽  
Author(s):  
Stephen Aichele ◽  
Paolo Ghisletta
Keyword(s):  
Depressive Symptoms ◽  
Sex Education ◽  
Structural Equation ◽  
Structural Equation Models ◽  
Memory Performance ◽  
Memory Deficits ◽  
Community Dwelling ◽  
Depression Symptoms ◽  
Age Related ◽  
Increased Risk

Abstract Objectives We examined bidirectional, time-ordered associations between age-related changes in depressive symptoms and memory. Method Data came from 107,599 community-dwelling adults, aged 49–90 years, who participated in the Survey of Health, Ageing, and Retirement in Europe (SHARE). Depressive symptoms were measured with the EURO-D inventory, and memory was evaluated as delayed recall of a 10-word list. Participants were assessed up to five times at 2-year intervals. Dynamic structural equation models were used to estimate longitudinal and time-ordered (lead-lag) relations between depressive symptoms and memory performance. Results Depressive symptoms increased and memory scores decreased across the observed age range, with worsening mostly evident after age 62 years. These long-term changes were moderately negatively correlated (r = −.53, p < .001). A time-ordered effect emerged such that age-specific memory deficits preceded shorter-term increases in depression symptoms. This effect can be translated such that each 1-point decrement on a 10-point memory scale at a given age predicted a 14.5% increased risk for depression two years later. Statistical adjustment for covariates (sex, education, re-test, smoking, and body mass index) had little influence on these associations. Conclusion In later adulthood, lower memory performance at a given age predicts subsequent 2-year increases in depressive symptoms.

scholarly journals APOE status and its association to learning and memory performance in middle aged and older Norwegians seeking assessment for memory deficits

2007 ◽  
Vol 3 (1) ◽  
pp. 57 ◽  
Author(s):  
Eike Wehling ◽  
Astri J Lundervold ◽  
Brit Standnes ◽  
Leif Gjerstad ◽  
Ivar Reinvang
Keyword(s):  
Learning And Memory ◽  
Memory Performance ◽  
Memory Deficits ◽  
Middle Aged
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