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Citation: Monica S, Anabela P and Rui C. The Continuing Challenge of Cognitive Decline: An Individual Process
of Aging?. Austin Alzheimers J Parkinsons Dis. 2015; 2(1): 1024.
Austin Alzheimers J Parkinsons Dis - Volume 2 Issue 1 - 2015
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Monica et al. © All rights are reserved
Austin Alzheimer’s and Parkinson’s Disease
Open Access
Abstract
During the modern gerontology the cognitive decline were generally
considered as an inevitable and natural accompaniment of aging. Over the past
decade, the distinction between normative from non-normative changes remains
difcult. The purpose of this review is to present a synthesis and integration
of the current knowledge of cognitive decline by interdisciplinary perspectives.
The theories of cognitive decline based on neuroplasticity and the predictors of
cognitive decline are also discussed. In addition, highlights current strengths
and limitations of the cognitive decline studies are critically analyzed.
Current researches are contesting the discouraging perspective that
assumes that the cognitive decline is related to normal process of aging across
the life span. The view that aging is a synonym of cognitive decline is being
replaced by the recognition that it is a multidimensional and multidirectional
process. However, cognitive decline is still not well understood.
Presently, rm conclusions about if the cognitive decline is a part of the
normal process of aging or just an individual process do not exist, there are only
speculations. The empirical ndings are heterogeneous and the resolution may
reside on interdisciplinary robust research.
Keywords: Cognitive decline; Aging; Risk factors; Protective factors;
Neuroplasticity
e cognitive reserve hypothesis and the theories of cognitive
based on neuroplasticity suggests that the brain has the capacity to
adapt to the process of aging, namely the response to the decrease
of cognitive abilities and sensory-motor, but also to the physical,
cognitive and social environment changes [9-12]. ere is a growing
tendency to considerer that the brain displays certain plasticity. For
this reason, some older adult maintain a good cognitive performance,
others experience decline in certain cognitive abilities [5,9,13].
In addition, the theory of biocultural co-constructivism consider
that the structure and function of the human brain is shaped with
the reciprocal action of co morbidities, the genes, the physical, the
cognitive and the social environment [9,13], and also to disclose that
each personal variables will interfere in the rate of changes as well as
aect dierently the process of aging [6-8,14,15]. In fact, the reasons
regarding cognitive decline has still not been fully understood.
In this review, we will critically discuss the emerging trends and
the developments of interdisciplinary research aiming to explore if
the cognitive decline is a part of the normal process of aging or just an
individual process, characterized by the individual specicities.
Overview of the cognitive decline in neuroscience and
psychology
Aging, brain and cognition: Aging is an inescapable natural
biologic process, regulated by genetic factors and inuenced by
environmental factors [13,15,16]. Successful aging for older adults is
dened as the absence of physical and mental disease or disability that
is associated with subjective perspectives of aging well [17].
Abbreviation
SCG: Subjective Cognitive Complain; AD: Alzheimer’s Disease;
MCI: Mild Cognitive Impairment; DSM-5: Diagnostic and Statistical
Manual of Mental Disorders - Fih Edition.
Introduction
e well-known demographic changes on Western societies
related to the aging of the population due to the progresses in medical
advances and technology used to treat a vast variety of problems,
which have increased the average of the life expectancy [1]. is
will change dramatically the age distribution in the next y years,
where the people of age 65 and older constitute a substantial part of
the population. For this reason, life course changes in the cognitive
abilities are an emergent phenomenon and a high priority scientic
challenge [2].
It is widely agreed that cognitive decline is a reduction in cognitive
abilities known as a normal part of aging [3] which has a negative
inuence on personal life and family functioning, as well as health
status, economic and healthcare repercussions [4,5]. Understanding
how to prevent and delay cognitive decline is important because these
decline can herald older adult who will suer from dementia in the
next decades and contribute signicantly to the reduction of costs of
caring for the individual, the family and the government [4,5].
e changes in cognitive function in human aging is not uniform
across the whole brain or all cognitive abilities, neither across all older
adult [6-8].
Review Article
The Continuing Challenge of Cognitive Decline: An
Individual Process of Aging?
Monica S*, Anabela P and Rui C
Department of Education, University of Aveiro, Portugal
*Corresponding author: Mónica S, Department of
Education, University of Aveiro, Campus Universitário de
Santiago, 383810-193 Aveiro, Portugal
Received: November 14, 2015; Accepted: December
23, 2015; Published: December 29, 2015
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ere is an ample evidence that life course concerns
neuroanatomical, morphologic biochemical and functional changes
who are intimately tied to alterations in cognitive function at dierent
stages in lifespan [16]. ese processes can lead to damage from
oxidative stress, diminished ability to detoxify free radicals, decline
in mitochondrial function, accumulation of amyloid-β peptide
and tau protein, decrease integrity of neuronal membranes, loss of
neurons and synapses, altered metabolic functions to cell death [18-
21]. e vast majority of imaging studies have suggested that notable
changes with healthy aging occurs markedly in frontal regions, but in
whole brain, particularly white matter volume, the prefrontal cortex,
hippocampus, sub cortical regions (thalamus, putamen, caudate,
nucleus accumbens) and parietal and temporal lobe volume, as
well as ventricular expansion, that is correlated with poor cognitive
performance[12,18,22]. ese changes may be related to gender.
In men, the frontal and temporal lobes are the most aected [23].
Whereas in women is the hippocampus and parietal lobes [18]. e
reduction of neurotransmitters has been also incorporated in the
normal aging process. is reduction on dopamine and acetylcholine
seems to be related with diculties in planning and small declines in
memory, respectively [12,19]. Studies using brain imaging techniques
and postmortem are considering the presence of inter individual
variability and providing evidences of neurodevelopmental arrests in
adulthood [23].
Over the past few years, a considerably evidence has been
accumulated suggesting that advancing chronological age is
associated by a systematic decline in many cognitive abilities that
play a prominent role. Over time, some cognitive abilities stabilize
and other may even increase. e uid abilities are the most aected
cognitive abilities by advancing of age [24]. As a matter of fact,
signicant changes in cognition can occur in multiple domains,
including the well-established episodic memory, attention, verbal
uency, processing speed, explicit memory, executive functions,
attention, working memory and language, which suer a substantial
decline thought much of adult age range [24]. Another important
consideration is that some aspects of cognition remains stable, or
even improves, across lifetime [25]. is is the case of crystallized
intelligence and emotion regulation [26]. For example, semantic
memory can remain stable throughout the life trajectory or, in some
cases, develop with age. In contrast with has been mentioned above,
the amygdala’s function is preserved in healthy older adults and
shows a minimal atrophy, as compared to other brain regions [12,26].
Relatively spared until late in life are knowledge-based verbal abilities
and verbal production, implicit memory and autobiographical
memory [27].
So far, the search of the study of this relationship between
volumetric cortical loss and cognitive decline aging has contradictory
results. It has been proposed that education and brain volume are
measures of cognitive reserve and predict slower progression to
cognitive decline [9,25]. Education, or intelligence itself, is also an
important protect factor for age-related changes that can impair
cognition [28]. In terms of life-course perceptive there is a continuum
between cognitive decits, childhood intelligence quotient and brain
cortical thickness [2], which may be a predictor of a successful
cognitive aging future and also reduce the chance of developing
vascular dementia [29]. For this reason, higher education level is
accompanied with greater cognitive performance [28], particularly in
executive and processing function [22]. is suggests that individuals
with successful coping with normal age-associated cognitive decline
are assumed to have higher cognitive reserve and develop a more
brain eciency throughout a more ecient use of brain networks
[16]. e opposite occur in the female gender, with less school years,
less levels of physical activity and depression [28,30]. ere is the
hypothesis, that education may inuence the cognitive trajectory by
promoting health consciousness, more physical exercise, better stress
management, meaningful social network and mentally-stimulating
activities [9,10,28].
e potential harbingers for future cognitive decline can be
the Subjective Cognitive Complain (SCG).e SCG may represent
a higher risk of progression to objective cognitive impairment or
neuropathologies and it is the earliest manifestation of Alzheimer
disease [31,32]. Recent ndings support that an objective
decline, whether self- or informant-based, are correlated with
greater psychological distress and could be an early indicator of
cognitive decline [31]. In fact, the clinical signicance remains
highly controversial because these complains are correlated with
psychological factors or are related to abnormal cerebrospinal uid
biomarkers of Alzheimer disease[33]. ese correlations make this
complain a clinical challenge to interpret. Apparently clinically
normal older adults with SCG can represent a unique opportunity
to study the natural course and history of Alzheimer disease but
also represent an important clue for early detection and preventive
interventions [31,32].
e complexity of brain, neural and cognitive function makes
the exact mapping of this cognitive decline extraordinarily dicult.
In fact, cognitive decline does not occur uniformly, whereas some
cognitive abilities are more susceptible aected than others to eects
of aging [23]. e etiology of the change, the chronological point when
this becomes evident, its magnitude and rate of progression varies
with cognitive function and among individuals [19]. Accordingly,
some older adults experience cognitive decline, others perform as well
or better than younger adults and the same individual may perform
dierently in dierent domains. e functional neuroimaging studies
reveals that owing to the normal processes of aging, the older adults
when compared to young people, exhibit more activity in the right
hemispheres, the ventral or dorsal prefrontal cortex during memory
tasks and the frontal and parietal throughout attention tasks [7,8,12].
According to the theories of neuroplasticity, it´s thinkable that older
adult may over recruited areas to compensate the weakness ones
[11,12]. Another possibility is that bilateral activation represents
a greater attentional eort a less selective cognitive processing or
can be related to an ineciency of sensory and perceptual abilities
[22]. An understanding of such processes not only are important
to the inferring neural plasticity and to how the development of
brain function across life, but can also be a source of insight into
the ways of this aging changes support the prism of adaptation.
Another controversial issue resides in neuronal regeneration. It is
hypothesized the development of dentate gyrus cells on hippocampus
[34]. However, the precise function and survival of these new cells is
still unknown.
e relationship between age-related changes in brain structure,
function and cognition are not uniform across the whole brain neither
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across all older adult [6-8]. e debate still exists to identify what is
cognitive decline and what is the underlying mechanism responsible
for those changes.
Predictors of cognitive decline: Several decades of research
revealed that biological, psychological, social engagement and lifestyle
can be regarded as predictors of cognitive decline [10,35].
e most cited risks factors are age, gender, education, objective
and subjective diculties like memory, reduced hippocampal size,
mood, personality (neuroticism), amyloid deposition, carrying one or
two apolipoprotein e4 alleles, presenilin-1 and presenilin-2, sensory
diculties, sedentary lifestyles, multiple medical comorbidities, and
nally, innumerous medical problems (hypertension and diabetes)
[20,21,36].
Relevant longitudinal and cross-sectional studies indicate that
chronological timetable aging is absent and the diseases processes
are independent of normal aging. It is noteworthy that aging increase
the risk for neurodegenerative diseases, vascular diseases (vascular
and micro vascular changes) [37], APOE-ε4 allele, stress-related
corticosteroid levels, lipid levels (cholesterol pathway) and chronic
inammation, which is associated as common brain abnormalities
in older adult [20]. Although changes in the bodies exists and were
marked by the decline over the time and these modications do not
inevitably lead to diseases such as diabetes or hypertension [38,39].
Besides that, the link between this variable and cognitive decline
has not been claried. It is plausible that the cognitive performance
decrements are associated with high arterial blood pressure, diabetes
mellitus, dyslipidemia, hypercholesterolemia, smoking, alcohol,
incident stroke or small vessel disease [36-39]. e association of
risk factors, brain lesion and cognition is complex. However, the
treatment of vascular risk factors can actually prevent or postpone
the cognitive decline and for the smokers the risk might be limited to
specic cognitive domains [37]. Preventing and diagnosis metabolic
and cardiovascular diseases might be essential to promote cognitively
healthy aging, but their applicability to research and clinical practice
is somewhat restricted.
Common or individual dierences in cognitive decline:
Implicit in the concept of healthy and successful aging is the idea
that the cognitive decline forms are continuum, so cognitive changes
associated to aging usually are in mild and do not interfere with
normal daily activities [17]. Oen, the distinction of normative
from non-normative changes remains dicult. On the one hand the
recognition of the predementia symptomatic stage of impartment
resulted in the identication of the Mild Cognitive Impairment
(MCI), as a transitional stage between normal aging and Alzheimer´s
Disease (AD) [40]. On the other hand, in dementia research there is a
long debate about if AD is an extreme of these continuum (continuity
view), presented in the revised diagnostic guidelines [3], or a category
dierent from normal ageing (discontinuity view) [5]. Recently,
reinforced by longitudinal studies, investigators started to consider
that the heterogeneity in cognitive decline across life time can reect
a variety of underlying neuropathological conditions. For this reason,
predicting the progressive to MCI, then to AD, versus the remittent
course of MCI in the primary care is so important. However, the
concept of MCI into clinical diagnostic algorithms, such as the
Diagnostic and Statistical Manual of Mental Disorders - Fih Edition
(DSM-5) [41], remains questionable, because three-quarters of
patients with MCI stayed cognitively stable or even improved within
3 years [42].
Cognitive decline cannot be considered unavoidable, it is not
known whether is, or not, an inevitable consequence of the advancing
of age [7,8,15]. e view that aging is a synonym of cognitive decline
is being replaced by the recognition that many individuals maintain
mental acuity even with the advance of age [7]. However, rm
conclusions about the etiology of the normal changes do not exist,
and there are only speculations.
It is abundantly clear that cognitive functioning are overlap
and interactive in a complex way and the evolution of cognitive
performance over the life-span is not a uniform process, but instead is
heterogeneous [7,8,15]. As summarized in (Figure 1), this variability
makes it dicult to predict a single prole of cognitive aging [43].
Current research is contesting that discouraging perspective
and claiming that signicant cognitive decline cannot be attributed
to age alone [16]. e answer for the biggest question for the
aging researchers is what accounts for this multidimensional and
multidirectional process of cognitive decline is the enormous inter-
individual variability (diversity) and intra-individual variability
(dispersion) [6,44]. In cognitive performance the diversity has been
associated with education, social engagement, economic resources
and genetic factors, whereas dispersion has been associated with
demographic, health and individual characteristics [44].
e biocultural co-constructivism theory suggests that the
brain and cognition abilities are shaped continually, not only in
early development, but also in adult life span [45].is emerging
trend of interdisciplinary research are making the rst steps in
Figure 1: Overview of individual cognitive decline for healthy and successful aging.
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the understanding that life span is co-constructed[46-48]. In fact,
according to this view, neurobehavioral development across the
life span are a reciprocal co-constructive interaction between
environment, culture, social context, behavioral, genetic, neural and
cognitive plasticity, and occurs simultaneously in the dierent time
scales (i.e., moment-to-moment micro genesis, life span ontogeny,
and human phylogeny) and encompassing multiple levels (i.e.,
neurobiological, cognitive, behavioral, and socio cultural), which
implies the diversity in the form of inter-individual dierence [48]
(Figure 2). For this reason, the individuals are not passive recipients
of their biological, ecological and cultural inheritances [46]. Instead
they are active agents and their behavior, memory plasticity, plasticity
of the functional organization of cognitive and cortical processes and
dopaminergic system inuence the development and organization of
their brain functional architecture [49]. e brain is an open, dynamic
and adaptive system that was personalized through lifespan [47].
e biocultural co-constructivism theory has been accumulating
empirical evidence; however details about reciprocal co-constructive
interactions are still not well understood [49].
e complex of the life span development and the large number
factors that inuences the rate of the cognitive aging between and
within individuals on an interactive and distinct way. Much of the
research continues to investigate the common factors that may
explain the overall population shi and those that dierentially aect
individuals [13,15]. Likewise, assume that cognitive decline has clear
generalities and common principles, but attributes this to variability
from individual to individual [6-8,14,15].
Limitation in cognitive decline studies: e determinants
of the cognitive aging across the life span are mainly explored by
diverse scientic areas like biomedical and psychological science.
e rapid and immense progress in the last decades have probably
provided ndings with several limitation, specically, (a) samples of
convenience have small sizes, which lessen the validity of any statistics
derived from them,(b) latent variables are commonly reported, (c)
group data poorly replicates the information about the individual
patient, (d) clinical groups with heterogeneous characteristics, (e)
reduced construct validity of the neuropsychological tests (measuring
more than one cognitive function), (f) short follow-up, and (g)
the possibility of undiagnosed the stage of pathological cognitive
impairment or reverse causation are present [2], [5,13,15].
e solution for those limitations may be in the addiction of
more disciplines, not only, medicine and psychology, but also
genetics, sociology, economics, epidemiology, education or even
communication [13]. Future research would benet with the
development of translational research methodologies, able to transfer
the results from a controlled laboratory studies to real life scenario.
In turn, this will improve each discipline and provide ambitious
and promising advance in understand deeper the complexity and
diversity of the life span.
Conclusion
At present, there are a number of questions that remains open.
e dierences between successful aging and age-related diseases are
poorly understood or have depressingly few answers. e reasons for
individual dierences on aging are a matter of considerable debate.
e key question phenomenon of cognitive decline needs some
agreement among the dierent theoretical perspectives of aging,
in order to determine the best methods to establish the dynamic
relationship between demographic, biological, social, environment
and personal factors. In view of the large limitations reported in the
study of cognitive decline, it seems necessary to explore and generate
new research hypotheses.
Firm understanding of the title of this article, e continuing
challenge of cognitive decline: an individual process of aging?,
hints to another important direction for the future research of
cognitive abilities in later adult life: the extraordinary opportunity
to the development of an cross-disciplinary investigation with the
integration or expansion of contemporary prospective cohort studies
with longer follow-up, in order to create a dierent epidemiological
study that may integrate a world-wide database about the course of the
evolution of human cognition. A better understanding has potential
targets like the interventions that could positively aect several
aspects of the life course changes in cognitive, prevent age-related
diseases and to improve active life expectancy and promote longevity
free of disease and disability. Besides engagement in physical, social
and cognitive activities, aging has potential for continued successful
development.
References
1. Draft C, Mortality GBD, Collaborators D, Burden TG, Gbd T, Goal-related
MD, et al. “Global, regional and national levels of age-specic mortality and
240 causes of death? A systematic analysis for the Global Burden of Disease
Study. 2013”. 2015; 1990-2013.
2. Karama S, Bastin ME, Murray C, Royle NA, Penke L, Maniega SM, et al.
“Childhood cognitive ability accounts for associations between cognitive
ability and brain cortical thickness in old age”. Mol. Psychiatry. 2014; 19: 555-
559.
Figure 2: Life span development by the view of biocultural co-constructivism theory.
Austin Alzheimers J Parkinsons Dis 2(1): id1024 (2015) - Page - 05
Monica S Austin Publishing Group
Submit your Manuscript | www.austinpublishinggroup.com
3. McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR, Kawas CH, et
al. “The diagnosis of dementia due to Alzheimer’s disease: Recommendations
from the National Institute on Aging-Alzheimer’s Association workgroups on
diagnostic guidelines for Alzheimer’s disease”. Alzheimer’s and Dementia.
2011; 7: 263-269.
4. Mason A, Lee R. “Population aging and generational economy project, a
global perspective”. In Population aging and the generational economy: key
ndings, L. R. and M. A., Eds. Cheltenham, UK, and Northampton, MA, USA:
Edward Elgar. 2011; 3-31.
5. Spaan PEJ, Dolan CV. “Cognitive decline in normal ageing and early
Alzheimer’s disease: A continuous or discontinuous transition?”. Behav.
Neurol. 2010; 23: 203-206.
6. Vaughan L, Leng I, Dagenbach D, Resnick SM, Rapp SR, Jennings JM, et
al. “Intraindividual variability in domain-specic cognition and risk of mild
cognitive impairment and dementia”. Curr. Gerontol. Geriatr. 2013; 2013:
495793.
7. Grady C. The cognitive neuroscience of ageing. Nat Rev Neurosci. 2012;
13: 491-505.
8. Grady CL. Cognitive neuroscience of aging. Ann N Y Acad Sci. 2008; 1124:
127-144.
9. Ballesteros S, Kraft E, Santana S, Tziraki C. Maintaining older brain
functionality: A targeted review. Neurosci Biobehav Rev. 2015; 55: 453-477.
10. Kuiper JS, Zuidersma M, Oude Voshaar RC, Zuidema SU, van den Heuvel
ER, Stolk RP, et al. “Social relationships and risk of dementia: A systematic
review and meta-analysis of longitudinal cohort studies”. Ageing Res. Rev.
2015; 22: 39-57.
11. Reuter-Lorenz PA, Cappell KA. “Neurocognitive aging and the compensation
hypothesis”. Current Directions in Psychological Science. 2008; 3: 177-182.
12. Kennedy KM, Rodrigue KM, Bischof GN, Hebrank AC, Reuter-Lorenz PA,
Park DC. “Age trajectories of functional activation under conditions of low and
high processing demands: An adult lifespan fMRI study of the aging brain”.
Neuroimage. 2015; 104: 21-34.
13. Falk EB, Hyde LW, Mitchell C, Faul J, Gonzalez R, Heitzeg MM, et al. “What
is a representative brain? Neuroscience meets population science”. Proc.
Natl. Acad. Sci. USA. 2013; 44: 17615-17622.
14. Glisky EL. “Changes in Cognitive Function in Human Aging”. 2007.
15. Deary IJ, Corley J, Gow AJ, Harris SE, Houlihan LM, Marioni RE, et al. “Age-
associated cognitive decline”. British Medical Bulletin. 2009; 92: 135-152.
16. Deary IJ, Penke L, Johnson W. The neuroscience of human intelligence
differences. Nat Rev Neurosci. 2010; 11: 201-211.
17. Reichstadt J, Geetika S, Colin A, Palinkas L, Dilip J, “Older Adults’
Perspectives on Successful Aging: Qualitative Interviews”. 2010; 18: 567-
575.
18. Peters R. Ageing and the brain. Postgrad Med J. 2006; 82: 84-88.
19. Dickstein DL, Weaver CM, Luebke JI, Hof PR. Dendritic spine changes
associated with normal aging. Neuroscience. 2013; 251: 21-32.
20. Gerritsen L, Comijs HC, Deeg DJH, Penninx BWJH, GeerlingsMI. “Salivary
cortisol, APOE-??4 allele and cognitive decline in a prospective study of older
persons”. 2011; 32: 1615-1625.
21. Wolk DA, Klunk W. Update on amyloid imaging: from healthy aging to
Alzheimer’s disease. Curr Neurol Neurosci Rep. 2009; 9: 345-352.
22. Goh JO, Beason-Held LL, An Y, Kraut MA, Resnick SM. “Frontal function and
executive processing in older adults: Process and region specic age-related
longitudinal functional changes”. 2013; 69: 43-50.
23. Bartzokis G, Beckson M, Lu PH, Nuechterlein KH, Edwards N, Mintz J. Age-
related changes in frontal and temporal lobe volumes in men: a magnetic
resonance imaging study. Arch Gen Psychiatry. 2001; 58: 461-465.
24. Tucker-Drob EM. Differentiation of cognitive abilities across the life span. Dev
Psychol. 2009; 45: 1097-1118.
25. Mazzonna F, Peracchi F. “Ageing, cognitive abilities and retirement,” Eur.
2012; 56: 691-710.
26. Urry H, Gross J. “Emotion Regulation in Older Age,” urrent Directions in
Psychological Science. 2010; 19: 352-357.
27. Holland CA, Ridout N, Walford E, Geraghty J. Executive function and
emotional focus in autobiographical memory specicity in older adults.
Memory. 2012; 20: 779-793.
28. Fratiglioni L, Winblad B, von Strauss E. Prevention of Alzheimer’s disease
and dementia. Major ndings from the Kungsholmen Project. Physiol Behav.
2007; 92: 98-104.
29. McGurn B, Deary IJ, Starr JM. Childhood cognitive ability and risk of late-
onset Alzheimer and vascular dementia. Neurology. 2008; 71: 1051-1056.
30. Luck T, Riedel-Heller SG, Luppa M, Wiese B, Wollny A, Wagner M, et al.
“Risk factors for incident mild cognitive impairment - Results from the
German Study on Ageing, Cognition and Dementia in Primary Care Patients
(AgeCoDe)”. 2010; 121: 260-272.
31. Blackburn DJ, Wakeeld S, Shanks MF, Harkness K, Reuber M, Venneri A.
Memory difculties are not always a sign of incipient dementia: a review of the
possible causes of loss of memory efciency. Br Med Bull. 2014; 112: 71-81.
32. Mendonça MD, Alves L, Bugalho P. From Subjective Cognitive Complaints
to Dementia: Who Is at Risk?: A Systematic Review. Am J Alzheimers Dis
Other Demen. 2015.
33. Wolfsgruber S, Jessen F, Koppara A, Kleineidam L, Schmidtke K, Frolich
L, et al. “Subjective cognitive decline is related to CSF biomarkers of AD in
patients with MCI”. 2015; 84: 1261-1268.
34. Lichtenwalner RJ, Parent JM. Adult neurogenesis and the ischemic forebrain.
J Cereb Blood Flow Metab. 2006; 26: 1-20.
35. Ngandu T, Lehtisalo J, Solomon A, Levälahti E, Ahtiluoto S, Antikainen R, et
al. “A 2 year multidomain intervention of diet, exercise, cognitive training, and
vascular risk monitoring versus control to prevent cognitive decline in at-risk
elderly people (FINGER): a randomised controlled trial”, Lancet. 2015; 385:
2255-2263.
36. Baumgart, Snyder HM, Carrillo MC, Fazio S, Kim H, Johns H. Summary of
the evidence on modiable risk factors for cognitive decline and dementia: A
population-based perspective. Alzheimers Dement. 2015; 11: 718-726.
37. Yaffe K, Vittinghoff E, Pletcher MJ, Hoang TD, Launer LJ, Whitmer R, et
al. Early adult to midlife cardiovascular risk factors and cognitive function.
Circulation. 2014; 129: 1560-1567.
38. Claassen JA. Cognitive decline and dementia: are we getting to the vascular
heart of the matter? Hypertension. 2015; 65: 505-506.
39. S Roriz-Filho J, Sá-Roriz TM, Rosset I, Camozzato AL, Santos AC, Chaves
ML, et al. (Pre) diabetes, brain aging, and cognition. Biochim Biophys Acta.
2009; 1792: 432-443.
40. Petersen RC, Doody R, Kurz A, Mohs RC, Morris JC, Rabins PV, et al.
Current concepts in mild cognitive impairment. Arch Neurol. 2001; 58: 1985-
1992.
41. American Psychiatric Association, Diagnostic and Statistical Manual of
Mental Disorders. American Psychiatric Association. 2013.
42. Kaduszkiewicz H, Eisele m, Wiese B, Prokein J, Luppa M, Luck T, et al.
“Prognosis of Mild Cognitive Impairment in General Practice: Results of the
German AgeCoDe Study”. 2014; 12: 158-165.
43. Duff K. “Mild Cognitive Impairment: Many Questions, Some Ansers”, in the
Neuropsychology of Cortical Dementias, C. Noggle and D. Raymond, Eds.
New York: Springer Publishing Company. 2015; 327-346.
44. Siegler RS. “Inter- and Intra-individual Differences in Problem Solving Across
the Lifespan”, in Lifespan Cognition Mechanisms of Change. 2006; 285-296.
45. Li S, Lindenberger U, Hommel B, Aschersleben G, Prinz w, Baltes PB.
“Transformations in the couplings among intellectual abilities and constituent
cognitive processes across the life span”. Psychol. Sci. a J. Am. Psychol.
2004; 15: 155-163.
Austin Alzheimers J Parkinsons Dis 2(1): id1024 (2015) - Page - 06
Monica S Austin Publishing Group
Submit your Manuscript | www.austinpublishinggroup.com
46. Li S. “Lifespan development of neuromodulation of adaptive control
and motivation as an ontogenetic mechanism for developmental niche
construction”, Developmental Science. 2013; 16: 317-319.
47. Li S. “Brain in macro experiential context: biocultural co-construction of
lifespan neurocognitive development”, Progress in Brain Research. 2009;
178: 17-29.
48. Li SC. Biocultural orchestration of developmental plasticity across levels: the
interplay of biology and culture in shaping the mind and behavior across the
life span. Psychol Bull. 2003; 129: 171-194.
49. Li S, Brehmer Y, Shing YL, Werkle-Bergner M, Lindenberger U.
“Neuromodulation of associative and organizational plasticity across the life
span: Empirical evidence and neurocomputational modeling,” Neuroscience
and Biobehavioral Reviews. 2006; 30: 775-790.
Citation: Monica S, Anabela P and Rui C. The Continuing Challenge of Cognitive Decline: An Individual Process
of Aging?. Austin Alzheimers J Parkinsons Dis. 2015; 2(1): 1024.
Austin Alzheimers J Parkinsons Dis - Volume 2 Issue 1 - 2015
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