Cited by 71Alzheimer's disease research and treatmentsFatty Acid Research and HealthDementia and Cognitive Impairment Research

Phospholipase A2 activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease

Schaeffer, Evelin L., Forlenza, Orestes V., Gattaz, Wagner F.·2009·Psychopharmacology

Abstract

Rationale Alzheimer disease (AD) is the leading cause of dementia in the elderly and has no known cure. Evidence suggests that reduced activity of specific subtypes of intracellular phospholipases A2 (cPLA2 and iPLA2) is an early event in AD and may contribute to memory impairment and neuropathology in the disease.Objective The objective of this study was to review the literature focusing on the therapeutic role of PLA2 stimulation by cognitive training and positive modulators, or of supplementation with arachidonic acid (PLA2 product) in facilitating memory function and synaptic transmission and plasticity in either research animals or human subjects.Methods MEDLINE database was searched (no date restrictions) for published articles using the keywords Alzheimer disease (mild, moderate, severe), mild cognitive impairment, healthy elderly, rats, mice, phospholipase A(2), phospholipid metabolism, phosphatidylcholine, arachidonic acid, cognitive training, learning, memory, long-term potentiation, protein kinases, dietary lipid compounds, cell proliferation, neurogenesis, and neuritogenesis. Reference lists of the identified articles were checked to select additional studies of interest.Results Overall, the data suggest that PLA2 activation is induced in the healthy brain during learning and memory. Furthermore, learning seems to regulate endogenous neurogenesis, which has been observed in AD brains. Finally, PLA2 appears to be implicated in homeostatic processes related to neurite outgrowth and differentiation in both neurodevelopmental processes and response to neuronal injury.Conclusion The use of positive modulators of PLA2 (especially of cPLA2 and iPLA2) or supplementation with dietary lipid compounds (e.g., arachidonic acid) in combination with cognitive training could be a valuable therapeutic strategy for cognitive enhancement in early-stage AD.

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Crossref · 10.1007/s00213-008-1351-0

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  • There is reason to believe that non-pharmacological approaches based on these novel findings might be beneficial to ameliorate Alzheimer's disease symptoms.

    “there is also reason to believe that non-pharmacological approaches based on these novel findings might be beneficial to ameliorate AD symptoms (Schaeffer et al., 2009).”

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Authors
Schaeffer, E. L., Forlenza, O. V., & Gattaz, W. F.
Affiliations
Universidade de São Paulo (BR)
Corresponding author
Schaeffer, Evelin L.
Venue
Psychopharmacology
Published
2008-10-14
Volume
202
Issue
1-3
Pages
37-51
ISSN
  • 0033-3158 (ISSN-L)
  • 1432-2072
OpenAlex
W2017563414
Cited by
71
References
179
Citations by year
2025: 1 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 1 · 2020: 5 · 2019: 2 · 2018: 1 · 2017: 5 · 2016: 6 · 2015: 5 · 2014: 7 · 2013: 6 · 2012: 6
FWCI
3.82
Type
journal article
Language
en
Open access
closed
Locations
  • Psychopharmacology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, phospholipase A2, calcium-dependent phospholipase A2, arachidonic acid, cognitive training, memory enhancement, synaptic plasticity, long-term potentiation, neurogenesis, neurite outgrowth, phospholipid metabolism, phosphatidylcholine, mild cognitive impairment, dietary fat supplementation, cognitive enhancement therapy
MeSH terms
Aged, Alzheimer Disease, Animals, Brain, Cells, Cultured, Cognition, Dietary Fats, Enzyme Activation, Humans, Learning, Memory Disorders, Neuronal Plasticity, Neurons, Amyloid beta-Peptides, Nootropic Agents, Cell Proliferation, Phospholipases A2

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