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{{Amnesia}}
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==Overview==
==Overview==
Amnesia results from damage to different memory centers in the brain, such as the [[medial temporal lobe]] and the [[hippocampus]], which are involved in acquiring and restoring memory.
[[Memory]] is the stored information in the [[hippocampal]] region of the [[brain]]. depending on the duration, [[memory]] is divided into short term and long term.
==Pathophysiology==
==Pathophysiology==
Memory is disrupted by damage that may occur in different parts of the brain such as the [[medial temporal lobe]], the [[hippocampus]], the [[cortex]] and the [[frontal lobe]].  Injury to any of these areas may lead to specific disruptions in the processes of acquiring and recalling memories. For instance, damage to the medial [[temporal lobe]] and [[hippocampus]] can sharply reduce the ability to acquire new [[declarative memory]] whereas damage to the storage areas in the cortex can disrupt retrieval of old memories and interfere with the acquisition of new memories.
===Physiology===
===Anterograde Amnesia===
[[Memory]] is the stored information in the [[hippocampal]] region of the [[brain]]. According to Richard Semon (1904), experiences cause some structural and functional changes in the [[neurons]] and these changes are referred to as ''engram'' and they form memory of that experience. Reactivation of these [[neurons]] occur when [[patient]] tries to recall those [[memories]].<ref>Semon R. (1904). Die mneme [The mneme]. Edited by W. Engelmann. Leipzig</ref> [[Memory]] is divided into groups depending on the duration:
Anterograde amnesia can result from damage to the [[hippocampal formation|hippocampus]], [[Fornix of brain|fornix]], or [[mammillary bodies]], thus lending credence to the theory that these structures are primarily responsible for laying down long-term memories. However, the condition can also arise from damage to the [[basal forebrain]] (which produces [[acetylcholine]]) or a set of brain structures called the [[diencephalon]].  
*[[Sensory]] [[memory]]: Information from around us is stored as [[sensory]] [[memory]].<ref name="pmid28713278">{{cite journal| author=Camina E, Güell F| title=The Neuroanatomical, Neurophysiological and Psychological Basis of Memory: Current Models and Their Origins. | journal=Front Pharmacol | year= 2017 | volume= 8 | issue=  | pages= 438 | pmid=28713278 | doi=10.3389/fphar.2017.00438 | pmc=5491610 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28713278  }} </ref>
===Dissociative or Functional or Psychogenic Amnesia===
*Short-term [[memory]] are for short period of time and use existing [[neuronal]] network.
There are three types of memory – sensory, short-term, and long-term memory. Sensory memory lasts up to hundreds of milliseconds and short-term memory lasts from seconds to minutes while anything else longer than short-term memory is considered to be a long-term memory.<ref name = Markowitsch>{{cite journal |author=Markowitsch HJ |title=Psychogenic amnesia |journal=Neuroimage |volume=20 Suppl 1 |issue= |pages=S132–8 |year=2003 |pmid=14597306 |doi=}}</ref><ref name = Reinhold/>
*Long-term [[memory]] are long lasting and are formed by structural/functional changes in [[neuronal]] network.<ref name="pmid25301080">{{cite journal| author=Bisaz R, Travaglia A, Alberini CM| title=The neurobiological bases of memory formation: from physiological conditions to psychopathology. | journal=Psychopathology | year= 2014 | volume= 47 | issue= 6 | pages= 347-56 | pmid=25301080 | doi=10.1159/000363702 | pmc=4246028 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25301080  }} </ref>


The information obtained from the [[peripheral nervous system]] (PNS) is processed in four stages - encoding, consolidating, storage, and retrieval.<ref name = Markowitsch/> During encoding, the limbic system is responsible for bottlenecking or filtering information obtained from the PNS. According to the type of information given, the duration of consolidating stage varies drastically. Majority of consolidated information gets stored in the cerebral cortical networks where the limbic system record episodic-autobiographical events. These stored episodic and semantic memories can be obtained by triggering the uncinate fascicle that interconnects the regions of the temporofrontal junction area.
===Pathogenesis===


Emotion seems to play an important role in memory processing in structures like the cingulated gyrus, the septal nuclei, and the amygdala that is primarily involved in emotional memories.<ref name = Markowitsch /><ref name = Yang>{{cite journal |author=Yang JC, Jeong GW, Lee MS, ''et al'' |title=Functional MR imaging of psychogenic amnesia: a case report |journal=Korean J Radiol |volume=6 |issue=3 |pages=196–9 |year=2005 |pmid=16145296 |doi=}}</ref> Functional imaging of normal patients reveal that right-hemisperic amygdala and ventral prefrontal regions are activated when they were retrieving autobiographical information and events. Additionally, the hippocampal region is known to be linked to recognizing faces.
{| class="wikitable"
Researchers have found that emotional memories can be suppressed in non-mentally ill individuals via the [[prefrontal cortex]] in two stages - an initial suppression of the sensory aspects of the memory, followed by a suppression of the [[emotion]]al aspect.<ref>{{cite journal |author=Depue BE, Curran T, Banich MT |title=Prefrontal regions orchestrate suppression of emotional memories via a two-phase process |journal=Science |volume=317 |issue=5835 |pages=215–9 |year=2007 |pmid=17626877 |doi=10.1126/science.1139560}}</ref>  It has also been proposed that [[glucocorticoid]]s can impair memory retrieval, though to date this has only been tested in rats.<ref>{{cite journal |author=Roozendaal B, de Quervain DJ, Schelling G, McGaugh JL |title=A systemically administered beta-adrenoceptor antagonist blocks corticosterone-induced impairment of contextual memory retrieval in rats |journal=Neurobiol Learn Mem |volume=81 |issue=2 |pages=150–4 |year=2004 |pmid=14990235 |doi=10.1016/j.nlm.2003.10.001}}</ref>
!align="center" style="background: #4479BA; color: #FFFFFF | '''Types of Amnesia'''
! align="center" style="background: #4479BA; color: #FFFFFF| '''Pathogenesis'''
|-
| [[Dissociative Amnesia]]        ||[[Psychological]] origin.
|-
|[[Transient global amnesia]] || Precipitated by [[brain]] [[ischemia]], [[migraine]], [[epileptic]] [[seizure]], [[venous]] [[congestion]], [[psychological]] [[trauma]].<ref name="pmid19031042">{{cite journal| author=Profice P, Rizzello V, Pennestrì F, Pilato F, Della Marca G, Sestito A | display-authors=etal| title=Transient global amnesia during transoesophageal echocardiogram. | journal=Neurol Sci | year= 2008 | volume= 29 | issue= 6 | pages= 477-9 | pmid=19031042 | doi=10.1007/s10072-008-1034-y | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19031042  }} </ref>
|-
| [[Post-traumatic Amnesia]] || Amnesia that follows [[head]] [[trauma]] could be temporary or permanent.<ref name="pmid11475324">{{cite journal| author=Leclerc S, Lassonde M, Delaney JS, Lacroix VJ, Johnston KM| title=Recommendations for grading of concussion in athletes. | journal=Sports Med | year= 2001 | volume= 31 | issue= 8 | pages= 629-36 | pmid=11475324 | doi=10.2165/00007256-200131080-00007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11475324  }} </ref>
|-
| [[Infantile]] Amnesia|| Influenced by cultural norms and [[sexual]] [[repression]].<ref name="pmid12653489">{{cite journal| author=Wang Q| title=Infantile amnesia reconsidered: a cross-cultural analysis. | journal=Memory | year= 2003 | volume= 11 | issue= 1 | pages= 65-80 | pmid=12653489 | doi=10.1080/741938173 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12653489  }} </ref>
|-
| [[Drug]]-Induced Amnesia||[[Benzodiazepine]] are the most common group of [[drugs]] that can cause [[drug]]-induced amnesia, especially if used with [[alcohol]].<ref> Sadock, Benjamin J., and Virginia A. Sadock. Kaplan & Sadock's concise textbook of clinical psychiatry. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Print</ref>
|-
| [[Neurologically]] Derived Amnesia|| [[Brain]] regions involved are the [[hippocampus]] and the [[medial]] [[temporal lobes]].<ref name="pmid29623196">{{cite journal| author=Allen RJ| title=Classic and recent advances in understanding amnesia. | journal=F1000Res | year= 2018 | volume= 7 | issue=  | pages= 331 | pmid=29623196 | doi=10.12688/f1000research.13737.1 | pmc=5861508 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29623196  }} </ref>
|-
| Amnesia in [[Korsakoff’s Syndrome]]|| Caused by [[thiamine]] [[deficiency]] due to prolonged [[alcohol]] use or severe [[malnutrition]]. [[Deficiency]] of [[thiamine]] damages medial [[thalamus]], [[mammillary bodies]] and causes [[cerebral atrophy]] due to lack of [[pyruvate]] [[decarboxylation]].<ref>Kolb, Bryan, and Ian Q. Whishaw. Fundamentals of human neuropsychology. New York, NY: Worth Publishers, 2003. Print.</ref>
|-
|[[Epileptic]] Amnesia|| Rare, episodic amnesia seen in [[patients]] with [[temporal lobe]] [[epilepsy]].<ref name="pmid21262589">{{cite journal| author=Walsh RD, Wharen RE, Tatum WO| title=Complex transient epileptic amnesia. | journal=Epilepsy Behav | year= 2011 | volume= 20 | issue= 2 | pages= 410-3 | pmid=21262589 | doi=10.1016/j.yebeh.2010.12.026 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21262589  }} </ref>
  |-
|[[Lacunar amnesia]]|| Occurs due to [[brain]] damage. These [[patients]] have a gap in [[memory]].<ref name="pmid747264">{{cite journal| author=Benezech M, Leyssenne JP| title=[Lacunar amnesia and criminal behaviour : realities and medico-legal consequences]. | journal=Ann Med Psychol (Paris) | year= 1978 | volume= 136 | issue= 6-8 | pages= 918-29 | pmid=747264 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=747264  }} </ref>
|}


Traumas can interfere with several memory functions. Dr. Bessel van der Kolk divided these functional disturbances into four sets, traumatic amnesia, global memory impairment, dissociative processes and traumatic memories' sensorimotor organization. Traumatic amnesia involves the loss of remembering traumatic experiences. The younger the subject and the longer the traumatic event is, the greater the chance of significant amnesia. Global memory impairment makes it difficult for these subjects to construct an accurate account of their present and past history. Dissociation refers to memories being stored as fragments and not as unitary wholes. Not being able to integrate traumatic memories seems to be the main element which leads to PTSD.  In the sensorimotor organization of traumatic memories, sensations are fragmented into different sensory components.<ref name="pmid8564271">{{cite journal |author=van der Kolk BA, Fisler R |title=Dissociation and the fragmentary nature of traumatic memories: overview and exploratory study |journal=J Trauma Stress |volume=8 |issue=4 |pages=505–25 |year=1995 |pmid=8564271 |doi= |url=http://www.trauma-pages.com/a/vanderk2.php | accessdate = 2008-03-22}}</ref>
==Genetics==
*[[Alzheimer's disease]]:<ref name="pmid21045163">{{cite journal| author=Bekris LM, Yu CE, Bird TD, Tsuang DW| title=Genetics of Alzheimer disease. | journal=J Geriatr Psychiatry Neurol | year= 2010 | volume= 23 | issue= 4 | pages= 213-27 | pmid=21045163 | doi=10.1177/0891988710383571 | pmc=3044597 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21045163  }} </ref>
**Late-onset: Apolipoprotein E (APOE) [[gene]] on [[chromosome]] 19. This [[gene]] has variable risk of developing [[Alzheimer's disease]] depending on the [[allele]]. APOE ε4 increases the risk, APOE ε3 neither increases nor decreases and APOE ε2 [[allele]] provides some protection against the [[disease]].
**Early-onset: [[Amyloid precursor protein]] (APP) on [[chromosome 21]], [[presenilin 1]] (PSEN1) on [[chromosome 14]] and [[presenilin 2]] (PSEN2) on [[chromosome 1]] are associated with early-onset [[Alzheimer's disease]].
*[[Deficiency]] of RbAp48 [[protein]] encoded by RBBP4 [[gene]] have been co-related to [[memory]] loss.<ref name="pmid23986399">{{cite journal| author=Pavlopoulos E, Jones S, Kosmidis S, Close M, Kim C, Kovalerchik O | display-authors=etal| title=Molecular mechanism for age-related memory loss: the histone-binding protein RbAp48. | journal=Sci Transl Med | year= 2013 | volume= 5 | issue= 200 | pages= 200ra115 | pmid=23986399 | doi=10.1126/scitranslmed.3006373 | pmc=4940031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23986399 }} </ref>
 
==Gross Pathology==
On gross pathology, generalized [[cortical atrophy]], more pronounced in [[hippocampus]] and [[medial temporal lobe]] is seen in [[patients]] with [[Alzheimer's disease]].<ref name="pmid31375134">{{cite journal| author=DeTure MA, Dickson DW| title=The neuropathological diagnosis of Alzheimer's disease. | journal=Mol Neurodegener | year= 2019 | volume= 14 | issue= 1 | pages= 32 | pmid=31375134 | doi=10.1186/s13024-019-0333-5 | pmc=6679484 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31375134  }} </ref>
 
==Microscopic Pathology==
*[[Korsakoff's syndrome]]:<ref name="pmid19066199">{{cite journal| author=Sullivan EV, Pfefferbaum A| title=Neuroimaging of the Wernicke-Korsakoff syndrome. | journal=Alcohol Alcohol | year= 2009 | volume= 44 | issue= 2 | pages= 155-65 | pmid=19066199 | doi=10.1093/alcalc/agn103 | pmc=2724861 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19066199  }} </ref>
**[[Gliosis]] and [[microhemorrhages]] found in [[periaqueductal]] and [[paraventricular]] region.,
**[[Mamillary bodies]] [[atrophy]] and
**[[Atrophy]] seen in [[thalamus]]
*[[Microscopic]] features seen in [[Alzheimer's disease]] are, [[amyloid plaques]], [[intracellular]] [[neurofibrillary tangles]], [[tau]]-positive [[neuropil threads]], [[dystrophic]] [[neurites]], activated [[microglia]], reactive [[astrocytes]], [[eosinophilic]] [[Hirano bodies]], [[granulovacuolar]] [[degeneration]] and [[cerebral]] [[amyloid]] [[angiopathy]].<ref name="pmid31375134">{{cite journal| author=DeTure MA, Dickson DW| title=The neuropathological diagnosis of Alzheimer's disease. | journal=Mol Neurodegener | year= 2019 | volume= 14 | issue= 1 | pages= 32 | pmid=31375134 | doi=10.1186/s13024-019-0333-5 | pmc=6679484 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31375134  }} </ref>


Psychogenic amnesia is far from being completely understood and while several explanations have been proposed, none of them have been verified as the mechanism that fits all types of psychogenic amnesia.  Different theories include:
* [[Psychoanalysis|Freudian psychology]] states that psychogenic amnesia is an act of self-preservation, an alternative to suicide.<ref name = Brandt>{{cite journal |author=Brandt J, Van Gorp WG |title=Functional ("psychogenic") amnesia |journal=Semin Neurol |volume=26 |issue=3 |pages=331–40 |year=2006 |pmid=16791779 |doi=10.1055/s-2006-945519}}</ref>
* [[Cognitive psychology|Cognitive]] point-of-view states that this disorder utilizes the body’s personal Semantics|semantic belief system to repress unwanted memories from entering the consciousness by altering [[neuropeptide]]s and [[neurotransmitter]]s released during stressful events, affecting the formation and recall of memory.<ref name = Brandt/>
* "Betrayal trauma theory suggests that psychogenic amnesia is an adaptive response to childhood abuse. When a parent or other powerful figure violates a fundamental ethic of human relationships, victims may need to remain unaware of the trauma not to reduce suffering but rather to promote survival. Amnesia enables the child to maintain an attachment with a figure vital to survival, development, and thriving. Analysis of evolutionary pressures, mental modules, social cognitions, and developmental needs suggests that the degree to which the most fundamental human ethics are violated can influence the nature, form, and processes of trauma and responses to trauma."<ref>{{cite journal |last=Freyd |first=J. |year=1994 |title=Betrayal Trauma: Traumatic Amnesia as an Adaptive Response to Childhood Abuse. |journal= Ethics & Behavior |volume=4 |issue=4 |pages=307–330 |url=http://www.questia.com/read/95814385 |accessdate= 2008-01-13 |doi=10.1207/s15327019eb0404_1}}</ref> 
*Normal autobiographical memory processing is blocked by imbalance or altered release of [[stress hormone]]s such as [[glucocorticoid]]s and [[mineralocorticoid]]s in the brain.<ref name = Markowitsch/><ref name = Yang/>  The regions of expanded [[limbic system]] in the [[Cerebral hemisphere|right hemisphere]] are more vulnerable to stress and trauma, affecting the body's [[opioid]]s, [[hormone]]s, and neurotransmitters such as [[norepinephrine]], [[serotonin]], and [[neuropeptide Y]].<ref name = Reinhold>{{cite journal | author = Reinhold, N | coauthors = Kuehnel, S, Brand, M & Markowitsch, HJ | title = Functional neuroimaging in memory and memory disturbances | journal = Current Medical Imaging Reviews | volume = 2 | issue = 1 | pages = 35–57 | year = 2006 | url = http://www.ingentaconnect.com/content/ben/cmir/2006/00000002/00000001/art00004 | accessdate = 2007-12-05 | doi = 10.2174/157340506775541668 }}</ref>  Increased levels of glucocorticoid and mineralocorticoid receptor density may affect the anterior temporal, [[orbitofrontal cortex]], [[Hippocampus|hippocampal]], and [[amygdala]]r regions. These morphological changes may be caused by loss of regulation of [[gene expression]]s in those receptors along with inhibition of neurotrophic factors during chronic stress conditions.
*[[Stress (medicine)|Stress]] may directly affect the medial [[Temporal lobe|temporal]]/[[Diencephalon|diencephalic]] system, inhibiting the retrieval of autobiographical memories and producing a loss of personal identity.  [[Negative feedback]] produced by this system may dampen the patient's emotions, giving a perplexed or 'flat' appearance.<ref name = Kopelman>{{cite journal |author=Kopelman MD |title=Disorders of memory |journal=Brain |volume=125 |issue=Pt 10 |pages=2152–90 |year=2002 |pmid=12244076 |doi=|url = http://brain.oxfordjournals.org/cgi/content/full/125/10/2152 | accessdate = 2008-04-05}}</ref>
==References==
==References==
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{{reflist|2}}
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Overview

Memory is the stored information in the hippocampal region of the brain. depending on the duration, memory is divided into short term and long term.

Pathophysiology

Physiology

Memory is the stored information in the hippocampal region of the brain. According to Richard Semon (1904), experiences cause some structural and functional changes in the neurons and these changes are referred to as engram and they form memory of that experience. Reactivation of these neurons occur when patient tries to recall those memories.[1] Memory is divided into groups depending on the duration:

Pathogenesis

Types of Amnesia Pathogenesis
Dissociative Amnesia Psychological origin.
Transient global amnesia Precipitated by brain ischemia, migraine, epileptic seizure, venous congestion, psychological trauma.[4]
Post-traumatic Amnesia Amnesia that follows head trauma could be temporary or permanent.[5]
Infantile Amnesia Influenced by cultural norms and sexual repression.[6]
Drug-Induced Amnesia Benzodiazepine are the most common group of drugs that can cause drug-induced amnesia, especially if used with alcohol.[7]
Neurologically Derived Amnesia Brain regions involved are the hippocampus and the medial temporal lobes.[8]
Amnesia in Korsakoff’s Syndrome Caused by thiamine deficiency due to prolonged alcohol use or severe malnutrition. Deficiency of thiamine damages medial thalamus, mammillary bodies and causes cerebral atrophy due to lack of pyruvate decarboxylation.[9]
Epileptic Amnesia Rare, episodic amnesia seen in patients with temporal lobe epilepsy.[10]
Lacunar amnesia Occurs due to brain damage. These patients have a gap in memory.[11]

Genetics

Gross Pathology

On gross pathology, generalized cortical atrophy, more pronounced in hippocampus and medial temporal lobe is seen in patients with Alzheimer's disease.[14]

Microscopic Pathology

References

  1. ↑ Semon R. (1904). Die mneme [The mneme]. Edited by W. Engelmann. Leipzig
  2. ↑ Camina E, Güell F (2017). "The Neuroanatomical, Neurophysiological and Psychological Basis of Memory: Current Models and Their Origins". Front Pharmacol. 8: 438. doi:10.3389/fphar.2017.00438. PMC 5491610. PMID 28713278.
  3. ↑ Bisaz R, Travaglia A, Alberini CM (2014). "The neurobiological bases of memory formation: from physiological conditions to psychopathology". Psychopathology. 47 (6): 347–56. doi:10.1159/000363702. PMC 4246028. PMID 25301080.
  4. ↑ Profice P, Rizzello V, Pennestrì F, Pilato F, Della Marca G, Sestito A; et al. (2008). "Transient global amnesia during transoesophageal echocardiogram". Neurol Sci. 29 (6): 477–9. doi:10.1007/s10072-008-1034-y. PMID 19031042.
  5. ↑ Leclerc S, Lassonde M, Delaney JS, Lacroix VJ, Johnston KM (2001). "Recommendations for grading of concussion in athletes". Sports Med. 31 (8): 629–36. doi:10.2165/00007256-200131080-00007. PMID 11475324.
  6. ↑ Wang Q (2003). "Infantile amnesia reconsidered: a cross-cultural analysis". Memory. 11 (1): 65–80. doi:10.1080/741938173. PMID 12653489.
  7. ↑ Sadock, Benjamin J., and Virginia A. Sadock. Kaplan & Sadock's concise textbook of clinical psychiatry. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Print
  8. ↑ Allen RJ (2018). "Classic and recent advances in understanding amnesia". F1000Res. 7: 331. doi:10.12688/f1000research.13737.1. PMC 5861508. PMID 29623196.
  9. ↑ Kolb, Bryan, and Ian Q. Whishaw. Fundamentals of human neuropsychology. New York, NY: Worth Publishers, 2003. Print.
  10. ↑ Walsh RD, Wharen RE, Tatum WO (2011). "Complex transient epileptic amnesia". Epilepsy Behav. 20 (2): 410–3. doi:10.1016/j.yebeh.2010.12.026. PMID 21262589.
  11. ↑ Benezech M, Leyssenne JP (1978). "[Lacunar amnesia and criminal behaviour : realities and medico-legal consequences]". Ann Med Psychol (Paris). 136 (6–8): 918–29. PMID 747264.
  12. ↑ Bekris LM, Yu CE, Bird TD, Tsuang DW (2010). "Genetics of Alzheimer disease". J Geriatr Psychiatry Neurol. 23 (4): 213–27. doi:10.1177/0891988710383571. PMC 3044597. PMID 21045163.
  13. ↑ Pavlopoulos E, Jones S, Kosmidis S, Close M, Kim C, Kovalerchik O; et al. (2013). "Molecular mechanism for age-related memory loss: the histone-binding protein RbAp48". Sci Transl Med. 5 (200): 200ra115. doi:10.1126/scitranslmed.3006373. PMC 4940031. PMID 23986399.
  14. ↑ 14.0 14.1 DeTure MA, Dickson DW (2019). "The neuropathological diagnosis of Alzheimer's disease". Mol Neurodegener. 14 (1): 32. doi:10.1186/s13024-019-0333-5. PMC 6679484 Check |pmc= value (help). PMID 31375134.
  15. ↑ Sullivan EV, Pfefferbaum A (2009). "Neuroimaging of the Wernicke-Korsakoff syndrome". Alcohol Alcohol. 44 (2): 155–65. doi:10.1093/alcalc/agn103. PMC 2724861. PMID 19066199.

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