Body memory

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Body memory (BM) is a hypothesis that the body itself is capable of storing memories, as opposed to only the brain. While experiments have demonstrated the possibility of cellular memory [1] there are currently no known means by which tissues other than the brain would be capable of storing memories. [2] [3]

Contents

Modern usage of BM tends to frame it exclusively in the context of traumatic memory and ways in which the body responds to recall of a memory. In this regard, it has become relevant in treatment for PTSD. [4]

Overview

Peter Levine calls BM implicit memory or more specifically procedural memory, things that the body is capable of doing automatically and not in one's consciousness. He clarifies 3 types of BM and frames his work in terms of traumatic memory consequence and resolution: [5]

  1. Learned motor actions - Action patterns that can be continuously modified over time by higher brain regions.
  2. Emergency response - Hardwired instinctual behaviors (i.e., fight or flight response, etc...).
  3. Attraction or repulsion - We are attracted to sources of nourishment and growth and repulsed from sources of injury or toxicity.

Nicola Diamond elaborates on the opinion of philosopher Merleau-Ponty and asserts that BM is formed by doing. Whether practicing a bodily activity or forming a reaction to a traumatic memory. [6]

Edward Casey speaks of BM as, "memory intrinsic to the body, how we remember by and through the body", rather than what is remembered about the body. [7]

Thomas Fuchs defines 6 different types of BM: procedural, situational, intercorporeal, incorporative, pain, and traumatic memory. He notes that they are not strictly separable from one another but "derived from different dimensions of bodily experience. [8] : 12  Michelle Summa further refines this definition as an implicit memory. A pre-thematic, operative consciousness of the past expressed through the body. [8] : 30 

Antonio Damasio calls these reactions to memories somatic markers or emotions that are expressed primarily as physical feelings. [9]

These memories are often associated with phantom pain in a part or parts of the body – the body appearing to remember the past trauma. The idea of body memory is a belief frequently associated with the idea of repressed memories, in which memories of incest or sexual abuse can be retained and recovered through physical sensations. [2] It may also be associated with phantom limb sensation but this is less common. [10]

Skepticism

In 1993, Susan E. Smith, presented a paper relating the idea of "Survivor Psychology" at a false memory syndrome conference, stated about BM that, "body memories are thought to literally be emotional, kinesthetic, or chemical recordings stored at the cellular level and retrievable by returning to or recreating the chemical, emotional, or kinesthetic conditions under which the memory recordings are filed. [2] She went on in the abstract of the paper, "one of the most commonly used theories to support the ideology of repressed memories or incest and sexual abuse amnesia is body memories." and "The belief in these pseudoscientific concepts appears to be related to scientific illiteracy, gullibility, and a lack of critical thinking skills and reasoning abilities in both the mental health community and in society at large" [2]

A 2017 systematic review of cross-disciplinary research in body memory found that the available data neither largely support or refute the claim that memories are stored outside of the brain and more research is needed. [11]

In the Encyclopedia of Phenomenology Embree notes that, "To posit body memory is to open up a Pandora's Box", and links the idea to physical associations of memory rather than as a memory stored in a bodily manner. [12]

Cellular memory

Cellular memory (CM) is a parallel hypothesis to BM positing that memories can be stored outside the brain in all cells. [13] The idea that non-brain tissues can have memories is believed by some who have received organ transplants, though this is considered impossible. The author said the stories are intriguing though and may lead to some serious scientific investigation in the future. [13] In his book TransplantNation Douglas Vincent suggests that atypical newfound memories, thoughts, emotions and preferences after an organ transplant are more suggestive of immunosuppressant drugs and the stress of surgery on perception than of legitimate memory transference. In other words, "as imaginary as a bad trip on LSD or other psychotropic drug." [14]

Cellular memory refers to the ability of cells to retain information about past states, exposures, or events and adapt their responses accordingly. This concept underpins various physiological and pathological processes, often mediated by hormonal pathways, feedback loops, and epigenetic mechanisms. The following are key examples illustrating the scientific basis of cellular memory.

Stress and emotional memory

The hypothalamic–pituitary–adrenal (HPA) axis, through the release of glucocorticoids like cortisol, plays a pivotal role in stress and emotional memory. Cortisol enhances the consolidation of emotionally charged memories by modulating hippocampal activity, yet it can impair memory retrieval. [15] This dual effect is supported by research showing that glucocorticoids improve consolidation of long-term memory, particularly for emotionally valenced information, while impairing retrieval processes. [16] Dysregulation of this pathway is implicated in stress-related disorders such as PTSD, where the over-consolidation of fear-based memories occurs. Studies have demonstrated that glucocorticoids facilitate memory encoding but may compromise the retrieval of information, creating a dynamic interplay between memory formation and stress responses.

Recent research has further elucidated how chronic stress shapes neural networks. Prolonged exposure to high cortisol levels can reduce hippocampal volume and inhibit neurogenesis, weakening the brain's capacity to form new memories while reinforcing maladaptive ones. [17] Those same studies have shown that chronic exposure to elevated cortisol levels, whether through stress or medical conditions, can lead to morphological changes in the hippocampus, suppress neuronal proliferation, and reduce hippocampal volume.

The dynamic interplay between memory formation and stress responses is evident in the research demonstrating that glucocorticoids facilitate memory encoding but may compromise the retrieval of information. [18] This relationship is thought to follow an inverted U-shaped curve, with optimal memory performance at moderate levels of cortisol and impairment at both low and high levels. [19] The differential activation of mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) at varying cortisol concentrations may explain this complex relationship between stress hormones and memory processes. [20]

Furthermore, the impact of glucocorticoids on memory is time-dependent and context-specific. While acute elevations in cortisol can enhance the consolidation of new memories, including extinction memories, chronic exposure to high cortisol levels may lead to detrimental effects on cognitive function. [21] This has important implications for the treatment of fear-related disorders, as glucocorticoid-based interventions may facilitate fear extinction by reducing the retrieval of aversive memories and enhancing the consolidation of extinction memories. [22]

Metabolic memory and nutritional states

Nutritional and metabolic states are encoded in cellular memory through hormonal and transcriptional mechanisms, including glucose-induced transcriptional hysteresis and thyroid hormone regulation. Prolonged hyperglycemia can induce lasting epigenetic changes in glucose-regulated pathways, contributing to long-term complications of diabetes, such as vascular damage and cognitive decline. [23] This phenomenon, known as "metabolic memory," involves persistent alterations in gene expression and cellular function even after normalization of glucose levels. [24]

Glucose-induced transcriptional hysteresis plays a significant role in this process. Studies have demonstrated that exposure to elevated glucose levels leads to a positive feedback loop, resulting in persistent expression of genes that promote glycolysis and inhibit alternative metabolic pathways. [25]

Similarly, during caloric deficits, the body adapts by lowering the basal metabolic rate and "remembering" prior energy-deprived states through alterations in leptin, ghrelin, and thyroid hormone signaling. These adaptive responses are examples of metabolic memory and highlight how previous nutritional environments shape cellular behavior. [26]

The concept of "memory" in hormonal states is indeed critical for maintaining metabolic homeostasis, but it can also lead to maladaptive outcomes in certain conditions. Chronic high glucose levels have been shown to alter epigenetic markers, leading to persistent vascular inflammation and oxidative stress. Transient hyperglycemia can induce long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells. [27] These changes persist for at least 6 days of subsequent normal glycemia, resulting in increased expression of pro-inflammatory genes such as monocyte chemoattractant protein 1 (MCP-1) and vascular cell adhesion molecule 1 (VCAM-1). [28]

The establishment of these epigenetic changes may precede cardiovascular complications and help predict vascular lesions in diabetic patients. [29] Importantly, these epigenetic marks may be transmitted across several generations, increasing the individual risk of disease. [30]

The concept of metabolic memory extends beyond glucose regulation. Nutritional and metabolic states are encoded in cellular memory through various hormonal and transcriptional mechanisms. [31] These mechanisms form a complex network that governs metabolic memory and can emerge as novel targets for both detection and intervention of metabolic diseases. [32]

Reproductive and developmental programming

Hormonal fluctuations during critical developmental periods, such as puberty or pregnancy, create lasting imprints on cellular and systemic physiology. These hormonal effects influence cognitive functions, secondary sexual characteristics, and susceptibility to hormone-sensitive disorders.

Early-life estrogen exposure has been associated with long-term changes in brain plasticity and memory capacity, contributing to gender differences in neuropsychiatric conditions. Estrogen plays a crucial role in brain development, particularly in determining central gender dimorphism. [33] During puberty and other developmental stages, estrogen-induced synaptic plasticity is evident, affecting neurotransmitter synthesis, release, and metabolism. [34]

Estrogen's effects on the central nervous system are multifaceted, involving both genomic and non-genomic mechanisms. These actions protect against a wide range of neurotoxic insults and influence electrical excitability, synaptic function, and morphological features. [35] Clinical evidence shows that estrogen withdrawal during the climacteric period leads to modifications in mood, behavior, and cognition, while estrogen administration can improve cognitive efficiency in post-menopausal women. [36]

Emerging studies indeed reveal that testosterone levels during puberty influence neural development, affecting synaptic pruning and myelination in the prefrontal cortex. These changes have long-term implications for decision-making, risk assessment, and emotional regulation. During adolescence, high testosterone levels are associated with increased anterior prefrontal cortex (aPFC) involvement in emotion control. [37]

Elevated glucocorticoids during maternal stress have been shown to alter fetal epigenetic markers. Maternal adversity during pregnancy, including stress, anxiety, and depression, is associated with increased maternal and fetal glucocorticoid concentrations, which can lead to long-term physiological and pathophysiological outcomes in offspring. [38] Studies have found a significant correlation between psychosocial maternal stress and offspring methylation at a specific CpG site in the exon 1F of the human glucocorticoid receptor gene NR3C1, which may predispose offspring to mood disorders and metabolic dysregulation. [39]

Flatworms

Biologists at Tufts University have been able to train flatworms despite the loss of the brain and head. This may show memory stored in other parts of the body in some animals. [40] A worm reduced to 1/279th of the original can be regrown within a few weeks and be trained much quicker to head towards light and open space for food, an unnatural behavior for a flatworm. With each head removed training times appear reduced. This may just be a sign of epigenetics showing the appearance of memory. [41]

However, in the 1950s and 1960s James McConnell flatworm experiments measured how long it took to learn a maze. McConnell trained some to move around a maze and then chopped them up and fed them to untrained worms. The untrained group learned faster compared to a control that had not been fed trained worms. McConnell believed the experiment indicated cellular memory. [42] The training involved stressing the worms with electric shock. This kind of stress releases persistent hormones and shows no evidence for memory transfer. Similar experiments with mice being trained and being fed to untrained mice showed improved learning. It was not a memory that was transferred but hormone enriched tissue. [42]

Current usage and research

In epigenetics there are various mechanisms for cells to pass on "memories" of stressors to their progeny. Strategies include Msn2 nucleo-cytoplasmic shuttling, changes in chromatin, partitioning of anti-stress factors, and damaged macromolecules between mother and daughter cells. [43]

In adaptive immunity there is a functional CM that enables the immune system to learn to react to pathogens through mechanisms such as cytoxic memory mediation in bone marrow, [44] innate immune memory in stromal cells, [45] fungal mediation of innate and inherited immunological response, [46] and T and B-cell immune training. [47] In this regard CM is essential for vaccine and immunity research.

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<span class="mw-page-title-main">Estrogen</span> Primary female sex hormone

Estrogen is a category of sex hormone responsible for the development and regulation of the female reproductive system and secondary sex characteristics. There are three major endogenous estrogens that have estrogenic hormonal activity: estrone (E1), estradiol (E2), and estriol (E3). Estradiol, an estrane, is the most potent and prevalent. Another estrogen called estetrol (E4) is produced only during pregnancy.

<span class="mw-page-title-main">Hypothalamus</span> Area of the brain below the thalamus

The hypothalamus is a small part of the vertebrate brain that contains a number of nuclei with a variety of functions. One of the most important functions is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. It forms the basal part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is about the size of an almond.

<span class="mw-page-title-main">Hypothalamic–pituitary–adrenal axis</span> Set of physiological feedback interactions

The hypothalamic–pituitary–adrenal axis is a complex set of direct influences and feedback interactions among three components: the hypothalamus, the pituitary gland, and the adrenal glands. These organs and their interactions constitute the HPS axis.

<span class="mw-page-title-main">Anterior pituitary</span> Anterior lobe of the pituitary gland

The anterior pituitary is a major organ of the endocrine system. The anterior pituitary is the glandular, anterior lobe that together with the makes up the pituitary gland (hypophysis) which, in humans, is located at the base of the brain, protruding off the bottom of the hypothalamus.

<span class="mw-page-title-main">Cortisol</span> Human natural glucocorticoid hormone

Cortisol is a steroid hormone in the glucocorticoid class of hormones and a stress hormone. When used as medication, it is known as hydrocortisone.

A maternal effect is a situation where the phenotype of an organism is determined not only by the environment it experiences and its genotype, but also by the environment and genotype of its mother. In genetics, maternal effects occur when an organism shows the phenotype expected from the genotype of the mother, irrespective of its own genotype, often due to the mother supplying messenger RNA or proteins to the egg. Maternal effects can also be caused by the maternal environment independent of genotype, sometimes controlling the size, sex, or behaviour of the offspring. These adaptive maternal effects lead to phenotypes of offspring that increase their fitness. Further, it introduces the concept of phenotypic plasticity, an important evolutionary concept. It has been proposed that maternal effects are important for the evolution of adaptive responses to environmental heterogeneity.

<span class="mw-page-title-main">Glucocorticoid</span> Class of corticosteroids

Glucocorticoids are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the glucocorticoid receptor that is present in almost every vertebrate animal cell. The name "glucocorticoid" is a portmanteau and is composed from its role in regulation of glucose metabolism, synthesis in the adrenal cortex, and its steroidal structure.

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Steroid hormone receptors are found in the nucleus, cytosol, and also on the plasma membrane of target cells. They are generally intracellular receptors and initiate signal transduction for steroid hormones which lead to changes in gene expression over a time period of hours to days. The best studied steroid hormone receptors are members of the nuclear receptor subfamily 3 (NR3) that include receptors for estrogen and 3-ketosteroids. In addition to nuclear receptors, several G protein-coupled receptors and ion channels act as cell surface receptors for certain steroid hormones.

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11β-Hydroxysteroid dehydrogenase enzymes catalyze the conversion of inert 11 keto-products (cortisone) to active cortisol, or vice versa, thus regulating the access of glucocorticoids to the steroid receptors.

<span class="mw-page-title-main">Glucocorticoid receptor</span> Receptor to which cortisol and other glucocorticoids bind

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<span class="mw-page-title-main">Effects of stress on memory</span> Overview of the effects of stress on memory

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<span class="mw-page-title-main">Sympathoadrenal system</span>

The sympathoadrenal system is a physiological connection between the sympathetic nervous system and the adrenal medulla and is crucial in an organism's physiological response to outside stimuli. When the body receives sensory information, the sympathetic nervous system sends a signal to preganglionic nerve fibers, which activate the adrenal medulla through acetylcholine. Once activated, norepinephrine and epinephrine are released directly into the blood by adrenomedullary cells where they act as the bodily mechanism for "fight-or-flight" responses. Because of this, the sympathoadrenal system plays a large role in maintaining glucose levels, sodium levels, blood pressure, and various other metabolic pathways that couple with bodily responses to the environment. During numerous diseased states, such as hypoglycemia or even stress, the body's metabolic processes are skewed. The sympathoadrenal system works to return the body to homeostasis through the activation or inactivation of the adrenal gland. However, more severe disorders of the sympathoadrenal system such as pheochromocytoma can affect the body's ability to maintain a homeostatic state. In these cases, curative agents such as adrenergic agonists and antagonists are used to modify epinephrine and norepinephrine levels released by the adrenal medulla.

Maternal fetal stress transfer is a physiological phenomenon in which psychosocial stress experienced by a mother during her pregnancy can be transferred to the fetus. Psychosocial stress describes the brain's physiological response to perceived social threat. Because of a link in blood supply between a mother and fetus, it has been found that stress can leave lasting effects on a developing fetus, even before a child is born. According to recent studies, these effects are mainly the result of two particular stress biomarkers circulating in the maternal blood supply: cortisol and catecholamines.

Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These changes can lead to transgenerational stress inheritance.

Sleep epigenetics is the field of how epigenetics affects sleep.

References

  1. ↑ Cosier, Susan (May 2015). "Could Memory Traces Exist in Cell Bodies?". scientificamerican.com. doi:10.1038/scientificamericanmind0515-14b . Retrieved 31 May 2018.
  2. 1 2 3 4 Smith, Susan E. (1993). "Body Memories: And Other Pseudo-Scientific Notions of "Survivor Psychology"". Issues in Child Abuse Accusations. 5. Retrieved 31 May 2018.
  3. ↑ Scott O Lilienfeld SO; Lynn SJ; Lohr JM, eds. (2002). Science and Pseudoscience in Clinical Psychology. The Guilford Press. ISBN   1-57230-828-1.
  4. ↑ Bessel van der Kolk, M.D. (25 September 2014). The Body Keeps the Score: Brain, Mind, and Body in the Healing of Trauma. Penguin Publishing Group. ISBN   978-1-101-60830-2.
  5. ↑ Peter A. Levine, Ph.D. (27 October 2015). Trauma and Memory: Brain and Body in a Search for the Living Past: A Practical Guide for Understanding and Working with Traumatic Memory. North Atlantic Books. ISBN   978-1-58394-995-5.
  6. ↑ Nicola Diamond (1 April 2013). Between Skins: The Body in Psychoanalysis - Contemporary Developments. Wiley. ISBN   978-0-470-77816-6.
  7. ↑ Edward S. Casey (15 September 2009). Remembering, Second Edition: A Phenomenological Study. Indiana University Press. p. 147. ISBN   978-0-253-11431-0.
  8. 1 2 Sabine C. Koch; Thomas Fuchs; Michela Summa (1 January 2012). Body Memory, Metaphor and Movement. John Benjamins Publishing. ISBN   978-90-272-1350-1.
  9. ↑ Francois Ansermet (24 April 2018). Biology of Freedom: Neural Plasticity, Experience, and the Unconscious. Taylor & Francis. ISBN   978-0-429-91143-9.
  10. ↑ Price, Elfed Huw (2006). "A critical review of congenital phantom limb cases and a developmental theory for the basis of body image". Consciousness and Cognition. 15 (2): 310–322. doi:10.1016/j.concog.2005.07.003. PMID   16182566. S2CID   165404.
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  13. 1 2 Carroll, Robert Todd. "cellular memory". skepdic.com. Retrieved 31 May 2018.
  14. ↑ TransplantNation. Douglas Vincent. pp. 9–. GGKEY:H80NKZZSRW7.
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  16. ↑ Roozendaal, Benno; Hahn, Emily L.; Nathan, Sheila V.; De Quervain, Dominique J.-F.; McGaugh, James L. (2004). "Glucocorticoid Effects on Memory Retrieval Require Concurrent Noradrenergic Activity in the Hippocampus and Basolateral Amygdala". The Journal of Neuroscience. 24 (37): 8161–8169. doi:10.1523/JNEUROSCI.2574-04.2004. PMC   6729799 . PMID   15371517.
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  18. ↑ Rimmele, Ulrike; Besedovsky, Luciana; Lange, Tanja; Born, Jan (2013). "Blocking Mineralocorticoid Receptors Impairs, Blocking Glucocorticoid Receptors Enhances Memory Retrieval in Humans". Neuropsychopharmacology. 38 (5): 884–894. doi:10.1038/npp.2012.254. PMC   3671995 . PMID   23303058.
  19. ↑ Rimmele, Ulrike; Besedovsky, Luciana; Lange, Tanja; Born, Jan (2013). "Blocking Mineralocorticoid Receptors Impairs, Blocking Glucocorticoid Receptors Enhances Memory Retrieval in Humans". Neuropsychopharmacology. 38 (5): 884–894. doi:10.1038/npp.2012.254. PMC   3671995 . PMID   23303058.
  20. ↑ Rimmele, Ulrike; Besedovsky, Luciana; Lange, Tanja; Born, Jan (2013). "Blocking Mineralocorticoid Receptors Impairs, Blocking Glucocorticoid Receptors Enhances Memory Retrieval in Humans". Neuropsychopharmacology. 38 (5): 884–894. doi:10.1038/npp.2012.254. PMC   3671995 . PMID   23303058.
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  23. ↑ Ceriello, Antonio; Ihnat, Michael A.; Thorpe, Jessica E. (2009). "The "Metabolic Memory": Is More Than Just Tight Glucose Control Necessary to Prevent Diabetic Complications?". The Journal of Clinical Endocrinology & Metabolism. 94 (2): 410–415. doi:10.1210/jc.2008-1824. PMID   19066300.
  24. ↑ Mobbs, C. V. (2018). "Glucose-Induced Transcriptional Hysteresis: Role in Obesity, Metabolic Memory, Diabetes, and Aging". Frontiers in Endocrinology. 9: 232. doi: 10.3389/fendo.2018.00232 . PMC   5985453 . PMID   29892261.
  25. ↑ Mobbs, C. V. (2018). "Glucose-Induced Transcriptional Hysteresis: Role in Obesity, Metabolic Memory, Diabetes, and Aging". Frontiers in Endocrinology. 9: 232. doi: 10.3389/fendo.2018.00232 . PMC   5985453 . PMID   29892261.
  26. ↑ Dong, Hao; Sun, Yuezhang; Nie, Lulingxiao; Cui, Aimin; Zhao, Pengfei; Leung, Wai Keung; Wang, Qi (2024). "Metabolic memory: Mechanisms and diseases". Signal Transduction and Targeted Therapy. 9 (1): 38. doi:10.1038/s41392-024-01755-x. PMC   10899265 . PMID   38413567.
  27. ↑ El-Osta, A.; Brasacchio, D.; Yao, D.; Pocai, A.; Jones, P. L.; Roeder, R. G.; Cooper, M. E.; Brownlee, M. (2008). "Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia". The Journal of Experimental Medicine. 205 (10): 2409–2417. doi:10.1084/jem.20081188. PMC   2556800 . PMID   18809715.
  28. ↑ El-Osta, A.; Brasacchio, D.; Yao, D.; Pocai, A.; Jones, P. L.; Roeder, R. G.; Cooper, M. E.; Brownlee, M. (2008). "Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia". The Journal of Experimental Medicine. 205 (10): 2409–2417. doi:10.1084/jem.20081188. PMC   2556800 . PMID   18809715.
  29. ↑ Salvatore, Marco; Schiano, Concetta; Benincasa, Giuditta; Napoli, Claudio (2020). "Differential epigenetic factors in the prediction of cardiovascular risk in diabetic patients". European Heart Journal - Cardiovascular Pharmacotherapy. 6 (4): 239–247. doi:10.1093/ehjcvp/pvz062. PMC   7363021 . PMID   31665258.
  30. ↑ Salvatore, Marco; Schiano, Concetta; Benincasa, Giuditta; Napoli, Claudio (2020). "Differential epigenetic factors in the prediction of cardiovascular risk in diabetic patients". European Heart Journal - Cardiovascular Pharmacotherapy. 6 (4): 239–247. doi:10.1093/ehjcvp/pvz062. PMC   7363021 . PMID   31665258.
  31. ↑ Dong, Hao; Sun, Yuezhang; Nie, Lulingxiao; Cui, Aimin; Zhao, Pengfei; Leung, Wai Keung; Wang, Qi (2024). "Metabolic memory: Mechanisms and diseases". Signal Transduction and Targeted Therapy. 9 (1): 38. doi:10.1038/s41392-024-01755-x. PMC   10899265 . PMID   38413567.
  32. ↑ Dong, Hao; Sun, Yuezhang; Nie, Lulingxiao; Cui, Aimin; Zhao, Pengfei; Leung, Wai Keung; Wang, Qi (2024). "Metabolic memory: Mechanisms and diseases". Signal Transduction and Targeted Therapy. 9 (1): 38. doi:10.1038/s41392-024-01755-x. PMC   10899265 . PMID   38413567.
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  34. ↑ Genazzani, Andrea Riccardo; Pluchino, Nicola; Luisi, Stefano; Luisi, Michele (2007). "Estrogen, cognition and female ageing". Human Reproduction Update. 13 (2): 175–187. doi:10.1093/humupd/dml042. PMID   17135285.
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