Memory and Executive Function in Aging and AD
Open accessAbstract
Memory decline in aging results from multiple factors that influence both executive function and the medial temporal lobe memory system. In advanced aging, frontal-striatal systems are preferentially vulnerable to white matter change, atrophy, and certain forms of neurotransmitter depletion. Frontal-striatal change may underlie mild memory difficulties in aging that are most apparent on tasks demanding high levels of attention and controlled processing. Through separate mechanisms, Alzheimer's disease preferentially affects the medial temporal lobe and cortical networks, including posterior cingulate and retrosplenial cortex early in its progression, often before clinical symptoms are recognized. Disruption of the medial temporal lobe memory system leads directly to memory impairment. Recent findings further suggest that age-associated change is not received passively. Reliance on reserve is emerging as an important factor that determines who ages gracefully and who declines rapidly. Functional imaging studies, in particular, suggest increased recruitment of brain areas in older adults that may reflect a form of compensation.
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The l-dlPFC is integral to higher-order cognition and modulates episodic memory in MCI by enhancing encoding and facilitating retrieval.
“l-dlPFC is integral to higher-order cognition (i.e., executive function) [10,11], which modulates episodic memory in MCI by way of enhancing encoding and facilitating retrieval [12–14].”
From A phase I trial of accelerated intermittent theta burst rTMS for amnestic MCI (2024) · cites this paper as [12]
The passage labeled Abstract (page unavailable) says that declining executive function impairs strategic processing at encoding and retrieval, supporting a general link between executive function and memory. It discusses age-associated frontal-striatal changes, but does not establish this mechanism specifically for the left dorsolateral prefrontal cortex or for people with MCI. (LLM, conf=0.86)
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- Authors
- Buckner, R. L.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Buckner, Randy L.
- ORCID
- Buckner, Randy L.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 44
- Issue
- 1
- Pages
- 195-208
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2078790263
- Cited by
- 1,508
- References
- 19
- Citations by year
- 2026: 34 · 2025: 52 · 2024: 52 · 2023: 51 · 2022: 83 · 2021: 69 · 2020: 73 · 2019: 99 · 2018: 85 · 2017: 83 · 2016: 105 · 2015: 73 · 2014: 88 · 2013: 75 · 2012: 88
- FWCI
- 5.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (P01 AG05681, P01 AG0 3991, P01AG003991)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Cognitive Functions and Memory
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- executive function, Alzheimer's disease, brain atrophy, neurotransmitter depletion, attention, controlled processing, posterior cingulate cortex, retrosplenial cortex, cognitive reserve, neural compensation
- MeSH terms
- Aging, Alzheimer Disease, Animals, Humans, Memory
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