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The concept of retrogenesis in Alzheimer's disease/Conceptul de retrogeneza in boala Alzheimer.

INTRODUCTION

Justification of the Topic

The topic chosen to be discussed is one of great interest, if we take into consideration the fact that the increase in the absolute and relative number of elderly people will be accompanied by a significant rise of the number of people with Alzheimer's disease (AD). The estimated number of people with dementia worldwide is 24.3 million, with 4.6 million new cases of dementia every year (about one new case every seven seconds). The number of people living with dementia will almost double every 20 years, to 42.3 million in 2020 and 81.1 million in 2040 (1). In this regard, it would be necessary to explore new ways of understanding AD, which may help us to improve the management of this growing medical, social and economic problem.

Historical Background

General relationships between aging and development have long been noted by poets and playwrights. Aristophanes (423 B.C.) noted in his play The Clouds, that "old men are children twice over". In Shakespeare's comedy, "As you like it", Jacque's "All the world's a stage" soliloquy concludes that the "Last scene of all, That ends this strange, eventful history/Is second childishness ..." (2, 3) More than two centuries ago, physicians also began to note similarities between AD and normal development, as follows: "I met with an instance of a woman between 80 and 90 who exhibited the marks of a second infancy, by such a total decay of her mental faculties as to lose all consciousness in discharging her alvine and urinary excretions." (Benjamin Rush, 1793) (2, 3, 4) In the 1960s and 1970s, de Ajuriaguerra and his associates observed that the decline of certain capacities in dementia appeared to reverse Piaget's developmental stages (2, 3).

Definition of Retrogenesis

Retrogenesis has been defined by Reisberg and collaborators as the process by which the degenerative mechanisms from AD inversely recapitulate the processes of the normal neurodevelopment (2,5).

Functional Retrogenesis

The Functional Assessment Staging (FAST) procedure describes a total of 16 successive functional stages and substages in the continuum from normal aging to the late phase of AD (4, 6). The clinical retrogenic pattern in AD is most clearly described with the FAST staging procedure, as the sequence of functional loss outlined with the FAST appears to be a precise reversal of the order of acquisition of the same functions in the course of normal human development. It has also been noted that each FAST stage in AD can be described in terms of a corresponding developmental age (DA) (3,5,6,7,8,9)

Cognitive Retrogenesis

It was reported that the use of the adapted and modified Ordinal Scales of Psychological Development (OPSD), originally developed by Uzgiris & Hunt (1975) for cognitive testing in infants, has proved to be superior to the application of traditional tests, such as the MiniMental State Examination (MMSE), in assessing the residual cognitive capacity of subjects with moderately severe and severe AD (10, 11). Childhood intelligence test measures, such as the Tanaka--Binet intelligence scale (the Japanese version of the Binet scale), also proved to be useful in assessing cognition in moderate to severe AD subjects (12). Conversely, it was demonstrated that the MMSE, a standard AD measurement, is a suitable instrument for screening higher mental function in children at the age of 4 years and above (13).

Emotional Retrogenesis

The emotional and behavioral changes in the person with AD are frequently similar to those experienced by infants and children at corresponding DAs (3). For instance, it was noted that a FAST stage 6 AD person who is frustrated or mistreated will respond with verbal and physical outbursts, just as a 2- to 5-year-old child will respond with temper tantrums (3, 7, 14).

Neurologic Retrogenesis

It was observed that developmental reflexes (synonyms: infantile, neonatal or primitive reflexes) reappear in the AD person. Studies indicated that developmental reflexes emerge in AD at a point which might be anticipated from the corresponding DA and appear to be just as robust markers of the degenerative course of AD as of normal human development (6, 7, 15, 16, 17, 18). It was also noted that the emergence and increase of paratonia in AD can, to some extent, be considered as the return of an infantile stabilization reflex mechanism, which parallels the patient's decline in motor performance (19).

Neuropathologic Retrogenesis

It was indicated that the brain areas which are myelinated early in life become increasingly more thickly myelinated as time progresses, while the most recently myelinated ones have the least myelin deposition (2). Consequently, the developmentally most recent, thinly myelinated, brain regions are the most vulnerable to AD pathology (7).

Neurometabolic Evidence for Retrogenesis

A leading investigator in neurometabolism noted the similarities between the pattern of neurometabolism in normal infant brain and the pattern of neurometabolic deficit in late-stage AD brain (20, 21). It was also found that the regions of the brain which were most metabolically active in the default (awake, resting) states in young adults were the most vulnerable to the AD pathology (22).

Evidence from Tau Phosphorylation

It was observed that the extent and the sites of phosphorylation in tau from human fetal brains and tau from paired helical filaments in AD brains are similar, which suggests that the abnormal phosphorylation of tau in AD may be the result of reactivation of pathways governing the phosphorylation of tau in the developing brain (23, 24).

Electroencephalographic Evidence for Retrogenesis

It was revealed an important diagnostic value of electroencephalography (EEG) in the estimation of the severity of AD parallel to psychometric scales (25). It seems that EEG could be a predictor of the progression of AD (25, 26). Further data implicate EEG as a potential tool for differential diagnosis of AD from various dementing illnesses (26). In addition, studies reported that flicker at 10 Hz (a frequency near to the peak power of endogenous alpha) can enhance recognition memory by eliciting alpha-like EEG activity (27, 28). Furthermore, it was defined in detail an EEG retrogenic model showing that the EEG activity patterns in AD inversely recapitulate the patterns in normal development --such a model could be relevant for a better understanding of the nature of AD (29). A further implication of these findings is that EEG might be useful as a routine examination for AD patients.

A Science of Alzheimer's Disease Care Based on Retrogenesis

An understanding of the retrogenic process in AD also provides the basis for a detailed management science. This new science of AD care can be formulated into axioms, postulates and caveats. The care axioms are self-evident basic human needs and desires, such as those for dignity, accomplishment, social acceptance, love and movement, applicable to all human beings and to AD patients at all stages. The postulates are testable hypotheses of AD patient care based on the DA-retrogenesis model. Finally, the caveats are exceptions to the DA-retrogenesis model, based on the nature of human aging and AD (2, 8).

CONCLUSIONS

By describing several retrogenic models, the present paper provides new ways of understanding AD in order to improve the management of this very common disorder of later life. Thus, the final purpose would be to make the concept of retrogenesis to become both widely accepted and practically useful in the care of AD individuals.

Liana Rada Borza--M. D., Ph. D., Psychiatrist, Private Practice, Iasi, Romania

ACKNOWLEDGMENTS AND DISCLOSURE

The author declares he has no potential conflicts of interest to disclose.

REFERENCES

(1.) Ferri, C. P., Prince, M., Brayne, C. et al. Global prevalence of dementia: a Delphi consensus study. Lancet 2005; 366(9503): 2112-2117

(2.) Reisberg, B., Franssen, E. H., Souren, L. E., Auer, S. R., Akram, I. et al. Evidence and mechanisms of retrogenesis in Alzheimer's and other dementias: management and treatment import. Am J Alzheimers Dis Other Demen 2002; 17(4): 202-212

(3.) Reisberg, B., Kenowsky, S., Franssen, E. H. et al. Towards a science of Alzheimer's disease management: a model based upon current knowledge of retrogenesis. Int Psychoger 1999; 11(1): 7-23

(4.) Reisberg, B., Ferris, S. H., de Leon, M. J., Crook, T. Age-associated cognitive decline and Alzheimer's disease: implications for assessment and treatment. In: Bergener, M., Ermin, M., Stahelin, H. (eds.) Thresholds in Aging. London: Academic Press, 1985, pp. 255-292

(5.) Reisberg, B., Franssen, E. H., Hasan, S. M. et al. Retrogenesis: clinical, physiologic, andpathologic mechanisms in brain aging, Alzheimer's and other dementingprocesses. Eur Arch Psychiatry Clin Neurosci 1999; 249 Suppl. 3: 28-36

(6.) Reisberg, B. Commentary on "Diagnosis of Alzheimer's disease: two decades of progress". Symptomatology and biomolecular basis of Alzheimer's: a synthesis. Alzheimers Dement 2005; 1(2): 102-106

(7.) Reisberg, B., Franssen, E. H., Souren, L. E., Auer, S., Kenowsky, S. Progression of Alzheimer's disease: variability and consistency: ontogenic models, their applicability and relevance. J Neural Transm Suppl 1998; 54: 9-20

(8.) Reisberg, B., Franssen, E. H., Souren, L. E., Kenowsky, S. et al. Alzheimer's disease. In: Flanagan, S. R., Zaretsky, H., Moroz, A. (eds.) Medical aspects of disability: a handbook for the rehabilitation professional, 4th Edition. Springer Pub. Co., 2011, pp. 25-64

(9.) Reisberg, B., Pattschull-Furlan, A., Franssen, E., Sclan, S. G., Kluger, A., Dingcong, L., Ferris, S. H. Dementia of the Alzheimer type recapitulates ontogeny inversely on specific ordinal and temporal parameters. In: Kostovic, I. et al. (eds.) Neurodevelopment, Aging and Cognition. Springer-Verlag New York, 1992, pp. 345-369

(10.) Auer, S. R., Sclan, S. G., Yaffee, R. A. et al. The neglected half of Alzheimer disease: cognitive and functional concomitants of severe dementia. J Am Geriatr Soc 1994; 42(12): 1266-1272

(11.) Sclan, S. G., Foster, J. R., Reisberg, B. et al. Application of Piagetian measures of cognition in severe Alzheimer's disease. Psychiatr J Univ Ott 1990; 15(4): 221-226

(12.) Shimada, M., Hayat, J., Meguro, K. et al. Correlation between functional assessment staging and the 'Basic Age' by the Binet scale supports the retrogenesis model of Alzheimer's disease: a preliminary study. Psychogeriatrics 2003; 3: 82-87

(13.) Ouvrier, R. A., Goldsmith, R. F., Ouvrier, S. et al. The value of the Mini-Mental State Examination in childhood: a preliminary study. J Child Neurol 1993; 8(2): 145-148

(14.) Reisberg, B., Auer, S. R., Monteiro, I. et al. A rational psychological approach to the treatment of behavioral disturbances and symptomatology in Alzheimer's disease based upon recognition of the developmental age. In: Brunello, N., Langer, S. Z., Racagni, G. (eds.) Mental disorders in the elderly: New therapeutic approaches. Int Acad Biomed Drug Res Basel, Karger, 1998, vol. 13, pp. 102-109

(15.) Franssen, E. H., Kluger, A., Torossian, C. L. et al. The neurologic syndrome of severe Alzheimer's disease. Relationship to functional decline. Arch Neurol 1993; 50(10): 1029-1039

(16.) Franssen, E. H. & Reisberg, B. Neurologic markers of the progression of Alzheimer's disease. Int Psychogeriatr 1997; 9 Suppl 1: 297-306

(17.) Franssen, E. H., Reisberg, B., Kluger, A. et al. Cognition-independent neurologic symptoms in normal aging and probable Alzheimer's disease. Arch Neurol 1991; 48(2): 148-154

(18.) Franssen, E. H., Souren, L. E., Torossian, C. L. et al. Utility of developmental reflexes in the differential diagnosis and prognosis of incontinence in Alzheimer's disease. J Geriatr Psychiatry Neurol 1997; 10(1): 22-28

(19.) Souren, L. E., Franssen, E. H., Reisberg, B. Neuromotor changes in Alzheimer's disease: implications for patient care. J Geriatr Psychiatry Neurol 1997; 10(3): 93-98

(20.) Phelps, M. E. PET: the merging of biology and imaging into molecular imagining. J Nucl Med 2000; 41(4): 661-681

(21.) Phelps, M. E. Positron emission tomography provides molecular imaging of biological processes. Proc Natl Acad Sci USA 2000; 97(16): 9226-9233

(22.) Buckner, R. L., Snyder, A. Z., Shannon, B. J. et al. Molecular, structural and functional characterization of Alzheimer's disease: Evidence for a relationship between default activity, amyloid and memory. J Neurosci 2005; 25(34): 7709-7717

(23.) Brion, J. P., Smith, C., Couck, A. M. et al. Developmental changes in tauphosphorylation: fetal tau is transiently phosphorylated in a manner similar to paired helical filament-tau characteristic of Alzheimer's disease. J Neurochem 1993; 61(6): 2071-2080

(24.) Kenessey, A. & Yen, S. H. The extent of phosphorylation of fetal tau is comparable to that of PHF-tau from Alzheimer paired helical filaments. Brain Res 1993; 629(1): 40-46

(25.) Kowalski, J. W., Gawel, M., Pfeffer, A. et al. The diagnostic value of EEG in Alzheimer disease: correlation with the severity of mental impairment. J Clin Neurophysiol 2001; 18(6): 570-575

(26.) Jeong, J. EEG dynamics in patients with Alzheimer's disease. Clin Neurophysiol 2004; 115(7): 1490-1505

(27.) Williams, J. H. Frequency--specific effects of flicker on recognition memory. Neuroscience 2001; 104(2): 283-286

(28.) Williams, J., Ramaswamy, D., Oulhaj, A. 10 Hzflicker improves recognition memory in older people. BMC Neurosci 2006; 7: 21

(29.) Borza, L., Reisberg, B., Astarastoae, V., Dascalu, C. (2010). An Electrophysiological Model of Retrogenesis. In: Tsolaki, M. (ed.). Proceedings of the 25 th International Conference of Alzheimer's Disease International. Medimond International Proceedings, Italy, pp. 25-30, ISBN: 978-88-7587-582-4

Correspondence:

LIANA RADA BORZA

"Socola" Clinical Psychiatric Hospital

No. 36 Sos. Bucium, code 700282, Iasi, Romania

Phone: +40 232 430 920/int. 122

E-mail: liana_borza@hotmail.com

Date of Submission: September, 19, 2013

Acceptance: December, 18, 2013

INTRODUCERE

Justificarea temei

Tema aleasa este una de mare interes, daca tinem seama de faptul ca cresterea numarului absolut si relativ al persoanelor varstnice va fi insotita de o crestere semnificativa a numarului de persoane cu boala Alzheimer (BA). Numarul estimat al persoanelor cu dementa la nivel mondial este de 24,3 milioane, cu 4,6 milioane de cazuri noi anual (aproximativ un caz nou la fiecare sapte secunde). Numarul persoanelor care sufera de dementa aproape ca se va dubla la fiecare 20 de ani, la 42,3 de milioane in 2020 si 81,1 milioane in 2040 (1). In acest sens, ar fi necesara explorarea de noi cai de intelegere a BA, care ne-ar putea ajuta sa imbunatatim managementul acestei probleme medicale, sociale si economice aflate in plina crestere.

Context istoric

Relatii generale intre imbatranire si dezvoltare au fost demult observate de catre poeti si dramaturgi. Aristofan (423 i. H.) nota in piesa sa Norii ca "batranii sunt copii a doua oara". In comedia lui Shakespeare, Cum va place, Jacques, in al sau monolog, "Lumea intreaga este o scena", concluzioneaza ca: "Ultima scena din toate, /Care incheie aceasta ciudata istorie plina de evenimente/Este a doua copilarie ..." (2, 3) Acum mai bine de doua secole, medicii, de asemenea, au inceput sa constate similaritati intre BA si dezvoltarea normala, dupa cum urmeaza: "Am intalnit cazul unei femei intre 80 si 90 de ani care manifesta semnele unei a doua copilarii printr-un declin global al facultatilor sale mentale, astfel incat pierduse complet controlul excretiei de urina si materii fecale." (Benjamin Rush, 1793) (2, 3, 4) In anii 1960 si 1970, de Ajuriaguerra si asociatii sai remarcau ca declinul anumitor capacitati in dementa parea a fi opusul stadiilor de dezvoltare propuse de Piaget (2, 3).

Definitia retrogenezei

Retrogeneza a fost definita de Reisberg si colaboratori drept procesul prin care mecanismele degenerative din BA recapituleaza, in ordine inversa, procesele neurodezvoltarii normale (2, 5).

Retrogeneza functionala

Scala Functional Assessment Staging (FAST) descrie un total de 16 stadii si substadii functionale succesive in continuumul de la imbatranirea normala la faza avansata a BA (4, 6). Patternul retrogenetic clinic in BA este descris cel mai clar prin procedeul de stadializare FAST, avand in vedere ca secventa pierderii functionale evidentiate de FAST pare a fi o inversare precisa a ordinii de achizitie a acelorasi functii in cursul dezvoltarii umane normale. S-a remarcat, de asemenea, ca fiecare stadiu FAST in BA poate fi descris in termenii unei varste de dezvoltare corespunzatoare (3, 5, 6, 7, 8, 9).

Retrogeneza cognitiva

S-a raportat ca utilizarea Scalelor Ordinale ale Dezvoltarii Psihologice, adaptate si modificate, elaborate initial de Uzgiris si Hunt (1975) pentru testarea cognitiva infantila, s-a dovedit a fi superioara aplicarii testelor traditionale, precum Mini-Mental State Examination (MMSE), in evaluarea capacitatii cognitive reziduale a subiectilor cu BA moderat-severa si severa (10, 11). Testele pentru masurarea inteligentei la copil, precum scala de inteligenta Tanaka-Binet (versiunea japoneza a scalei Binet), de asemenea, sau dovedit utile in evaluarea cognitiei la subiectii cu BA moderata spre severa (12). Pe de alta parte, s-a demonstrat ca MMSE, o metoda standard de masurare pentru BA, reprezinta un instrument potrivit de screening al functiei mentale superioare in cazul copiilor in varsta de peste 4 ani (13).

Retrogeneza emotionala

Schimbarile emotionale si comportamentale ale persoanei cu BA sunt, in mod frecvent, similare cu cele resimtite de sugari si copii cu varste de dezvoltare corespunzatoare (3). Spre exemplu, s-a constatat ca o persoana aflata in stadiul 6 al BA, care se simte frustrata sau tratata necorespunzator, va reactiona prin izbucniri verbale si fizice, tot asa cum un copil intre 2 si 5 ani va reactiona prin accese de furie (3, 7, 14).

Retrogeneza neurologica

S-a observat ca reflexele dezvoltarii (sinonime: reflexe infantile, neonatale sau primitive) reapar la persoana cu BA. Studiile indica faptul ca reflexele dezvoltarii apar in BA intr-un moment care poate fi anticipat dupa varsta de dezvoltare corespunzatoare si par a fi markeri la fel de robusti ai evolutiei degenerative a BA ca ai dezvoltarii umane normale (6, 7, 15, 16, 17, 18). S-a semnalat, de asemenea, ca manifestarea si accentuarea paratoniei in BA pot fi considerate, intr-o anumita masura, drept revenirea unui mecanism reflex infantil de stabilizare, care corespunde declinului performantei motrice a pacientului (19).

Retrogeneza neuropatologica

S-a indicat ca ariile cerebrale care sunt mielinizate devreme in cursul vietii devin din ce in ce mai gros mielinizate cu timpul, pe cand cele mielinizate cel mai recent prezinta cea mai mica depunere de mielina (2). In consecinta, regiunile cerebrale mielinizate cel mai recent din punct de vedere al dezvoltarii si cel mai subtire sunt cele mai vulnerabile fata de patologia BA (7).

Dovezi neurometabolice pentru retrogeneza

Un cercetator de varf in domeniul neurometabolismului nota similitudinile dintre pattern-ul neurometabolismului creierului de nou-nascut normal si pattern-ul deficitului neurometabolic al creierului afectat de BA in stadiu avansat (20, 21). S-a descoperit, de asemenea, ca regiunile cerebrale cele mai active din punct de vedere metabolic in starile de veghe (treaz, in repaus) la adultii tineri sunt cele mai vulnerabile fata de patologia BA (22).

Dovezi oferite de fosforilarea tau

S-a observat ca gradul si situsurile de fosforilare ale proteinei tau de la nivelul creierelor fetale umane si ale proteinei tau din cadrul perechilor de filamente elicoidale de la nivelul creierelor afectate de BA sunt similare, ceea ce sugereaza ca fosforilarea anormala a proteinei tau in BA ar putea fi rezultatul reactivarii cailor care guverneaza fosforilarea tau in creierul aflat in dezvoltare (23, 24).

Dovezi electroencefalografice pentru retrogeneza

S-a scos in evidenta importanta valoare diagnostica a electroencefalografiei (EEG) in estimarea severitatii BA in paralel cu scalele psihometrice (25). Se pare ca EEG ar putea fi un predictor al evolutiei BA (25, 26). Date suplimentare implica EEG drept un potential instrument pentru diagnosticul diferential al BA cu variate maladii care asociaza dementa (26). In plus, studiile au raportat ca stimularea luminoasa intermitenta de 10 Hz (o frecventa apropiata de puterea de varf a lui alfa endogen) poate imbunatati memoria de recunoastere prin inducerea unei activitati EEG similare ritmului alfa (27, 28). Mai mult, a fost definit in detaliu un model retrogenetic EEG care arata ca pattern-urile activitatii EEG din BA recapituleaza in ordine inversa pattern-urile din dezvoltarea normala--un asemenea model ar putea fi relevant pentru o mai buna intelegere a naturii BA (29). O alta implicatie a acestor rezultate este aceea ca EEG ar putea fi utila ca examinare de rutina la pacientii cu BA.

O stiinta a ingrijirii in boala Alzheimer bazata pe retrogeneza

Intelegerea procesului retrogenetic din BA, de asemenea, sta la baza unei stiinte detaliate de management. Aceasta noua stiinta a ingrijirii in BA poate fi formulata pe baza unor axiome, postulate si avertismente. Axiomele de ingrijire sunt nevoile si dorintele umane de baza, evidente, precum cele privind demnitatea, realizarea, acceptarea sociala, dragostea si miscarea, aplicabile tuturor fiintelor umane si tuturor pacientilor cu BA, indiferent de stadiul bolii. Postulatele sunt ipoteze testabile referitoare la ingrijirea pacientului cu BA, bazate pe modelul varsta de dezvoltare--retrogeneza. In cele din urma, avertismentele constituie exceptii de la modelul varsta de dezvoltare--retrogeneza, fundamentate pe natura imbatranirii umane si a BA (2, 8).

CONCLUZII

Prin descrierea de modele retrogenetice, prezenta lucrare ofera noi cai de intelegere a BA pentru a imbunatati managementul acestei maladii foarte comune la o varsta inaintata. Astfel, scopul final ar fi sa se faca in asa fel incat conceptul de retrogenega sa devina larg acceptat si util din punct de vedere practic in ingrijirea persoanelor cu BA.

Liana Rada Borza--M. D., Ph. D., Specialist Psihiatru, Practica privata, Iasi, Romania

MULTUMIRI SI DEVOALARI

Autorul declara ca nu are conflicte potentiale de interese de declarat in legatura cu acest articol.

BIBLIOGRAFIE

1. Ferri, C. P., Prince, M., Brayne, C. et al. Global prevalence of dementia: a Delphi consensus study. Lancet 2005; 366(9503): 2112-2117

2. Reisberg, B., Franssen, E. H., Souren, L. E., Auer, S. R., Akram, I. et al. Evidence and mechanisms of retrogenesis in Alzheimer's and other dementias: management and treatment import. Am J Alzheimers Dis Other Demen 2002; 17(4): 202-212

3. Reisberg, B., Kenowsky, S., Franssen, E. H. et al. Towards a science of Alzheimer's disease management: a model based upon current knowledge of retrogenesis. Int Psychoger 1999; 11(1): 7-23

4. Reisberg, B., Ferris, S. H., de Leon, M. J., Crook, T. Age-associated cognitive decline and Alzheimer's disease: implications for assessment and treatment. In: Bergener, M., Ermin, M., Stahelin, H. (eds.) Thresholds in Aging. London: Academic Press, 1985, pp. 255-292

5. Reisberg, B., Franssen, E. H., Hasan, S. M. et al. Retrogenesis: clinical, physiologic, and pathologic mechanisms in brain aging Alzheimer's and other dementingprocesses. Eur Arch Psychiatry Clin Neurosci 1999; 249 Suppl. 3: 28-36

6. Reisberg, B. Commentary on "Diagnosis of Alzheimer's disease: two decades of progress". Symptomatology and biomolecular basis of Alzheimer's: a synthesis. Alzheimers Dement 2005; 1(2): 102-106

7. Reisberg, B., Franssen, E. H., Souren, L. E., Auer, S., Kenowsky, S. Progression of Alzheimer's disease: variability and consistency: ontogenic models, their applicability and relevance. J Neural Transm Suppl 1998; 54: 9-20

8. Reisberg, B., Franssen, E. H., Souren, L. E., Kenowsky, S. et al. Alzheimer's disease. In: Flanagan, S. R., Zaretsky, H., Moroz, A. (eds.) Medical aspects of disability: a handbook for the rehabilitation professional, 4th Edition. Springer Pub. Co., 2011, pp. 25-64

9. Reisberg, B., Pattschull-Furlan, A., Franssen, E., Sclan, S. G., Kluger, A., Dingcong, L., Ferris, S. H. Dementia of the Alzheimer type recapitulates ontogeny inversely on specific ordinal and temporal parameters. In: Kostovic, I. et al. (eds.) Neurodevelopment, Aging and Cognition. Springer-Verlag New York, 1992, pp. 345-369

10. Auer, S. R., Sclan, S. G., Yaffee, R. A. et al. The neglected half of Alzheimer disease: cognitive and functional concomitants of severe dementia. J Am Geriatr Soc 1994; 42(12): 1266-1272

11. Sclan, S. G., Foster, J. R., Reisberg, B. et al. Application of Piagetian measures of cognition in severe Alzheimer's disease. Psychiatr J Univ Ott 1990; 15(4): 221-226

12. Shimada, M., Hayat, J., Meguro, K. et al. Correlation between functional assessment staging and the 'Basic Age' by the Binet scale supports the retrogenesis model of Alzheimer's disease: a preliminary study. Psychogeriatrics 2003; 3: 82-87

13. Ouvrier, R. A., Goldsmith, R. F., Ouvrier, S. et al. The value of the Mini-Mental State Examination in childhood: a preliminary study. J Child Neurol 1993; 8(2): 145-148

14. Reisberg, B., Auer, S. R., Monteiro, I. et al. A rational psychological approach to the treatment of behavioral disturbances and symptomatology in Alzheimer's disease based upon recognition of the developmental age. In: Brunello, N., Langer, S. Z., Racagni, G. (eds.) Mental disorders in the elderly: New therapeutic approaches. Int Acad Biomed Drug Res Basel, Karger, 1998, vol. 13, pp. 102-109

15. Franssen, E. H., Kluger, A., Torossian, C. L. et al. The neurologic syndrome of severe Alzheimer's disease. Relationship to functional decline. Arch Neurol 1993; 50(10): 1029-1039

16. Franssen, E. H. & Reisberg, B. Neurologic markers of the progression of Alzheimer's disease. Int Psychogeriatr 1997; 9 Suppl 1: 297-306

17. Franssen, E. H., Reisberg, B., Kluger, A. et al. Cognition-independent neurologic symptoms in normal aging and probable Alzheimer's disease. Arch Neurol 1991; 48(2): 148-154

18. Franssen, E. H., Souren, L. E., Torossian, C. L. et al. Utility of developmental reflexes in the differential diagnosis and prognosis of incontinence in Alzheimer's disease. J Geriatr Psychiatry Neurol 1997; 10(1): 22-28

19. Souren, L. E., Franssen, E. H., Reisberg, B. Neuromotor changes in Alzheimer's disease: implications for patient care. J Geriatr Psychiatry Neurol 1997; 10(3): 93-98

20. Phelps, M. E. PET: the merging of biology and imaging into molecular imagining. J Nucl Med 2000; 41(4): 661-681

21. Phelps, M. E. Positron emission tomography provides molecular imaging of biologicalprocesses. Proc Natl Acad Sci USA 2000; 97(16): 92269233

22. Buckner, R. L., Snyder, A. Z., Shannon, B. J. et al. Molecular, structural and functional characterization of Alzheimer's disease: Evidence for a relationship between default activity, amyloid and memory. J Neurosci 2005; 25(34): 7709-7717

23. Brion, J. P., Smith, C., Couck, A. M. et al. Developmental changes in tauphosphorylation: fetal tau is transiently phosphorylated in a manner similar to paired helical filament-tau characteristic of Alzheimer's disease. J Neurochem 1993; 61(6): 2071-2080

24. Kenessey, A. & Yen, S. H. The extent of phosphorylation of fetal tau is comparable to that of PHF-tau from Alzheimer paired helical filaments. Brain Res 1993; 629(1): 40-46

25. Kowalski, J. W., Gawel, M., Pfeffer, A. et al. The diagnostic value of EEG in Alzheimer disease: correlation with the severity of mental impairment. J Clin Neurophysiol 2001; 18(6): 570-575

26. Jeong, J. EEG dynamics in patients with Alzheimer's disease. Clin Neurophysiol 2004; 115(7): 1490-1505

27. Williams, J. H. Frequency--specific effects of flicker on recognition memory. Neuroscience 2001; 104(2): 283-286

28. Williams, J., Ramaswamy, D., Oulhaj, A. 10 Hz flicker improves recognition memory in older people. BMC Neurosci 2006; 7: 21

29. Borza, L., Reisberg, B., Astarastoae, V., Dascalu, C. (2010). An Electrophysiological Model of Retrogenesis. In: Tsolaki, M. (ed.) Proceedings of the 25th International Conference of Alzheimer's Disease International. Medimond International Proceedings, Italy, pp. 25-30, ISBN 978-88-7587-582-4

Corespondenta:

LIANA RADA BORZA

Spitalul Clinic de Psihiatrie "Socola" Iasi

Sos. Bucium nr. 36, cod 700282, Iasi, Romania

Tel.: +40 232 430 920/int. 122

E-mail: liana_borza@hotmail.com

Primit: Septembrie, 19, 2013

Acceptat: Decembre, 18, 2013
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Author:Borza, Liana Rada
Publication:Bulletin of Integrative Psychiatry
Article Type:Report
Date:Mar 1, 2014
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