JAHS 7 (2)■ REVIEW

The latest in dementia prevention:
A review of the promising role of aerobic exercise
Kenta Shigemori1)

1) Kansai University of Welfare Sciences
3-11-1 Asahigaoka, Kashiwara, Osaka, 582-0026, Japan
Tel: ＋81-72-978-0088 e-mail:kenta.shigemori@gmail.com

JAHS 7 (2): 37-45, 2016. Submitted Sep. 15, 2016. Accepted Sep. 25, 2016.

ABSTRACT:

Aerobic exercise (AE) has been widely acknowledged for improving brain health. In particular, AE
has a potent impact on promoting the function of the hippocampus. The potential for AE to be
applied as a therapeutic or adjunctive intervention for a range of human conditions appears
increasingly more promising. Augmenting existing treatment approaches using AE-based
interventions may promote hippocampal function. Moreover, incorporating non-pharmacologicalinterventions into clinical treatment may have several other benefits for the patient’s wellbeing.
This review incorporates both animal and human studies to comprehensively detail the associationof AE with cognitive enhancements.

Key words: Aerobic exercise (AE),

Alzheimer's disease (AD),INTRODUCTION

Brain healthpromoting the function of the hippocampus.
Thereistargetingdeficits
intheneuroplasticity of crucial areas to cognition likethe hippocampus, is a promising approach to
remediating
cognitive
dysfunction.
The
potential for AE to be applied as a therapeuticor adjunctive intervention for a range of humanconditions
appearsincreasingly
morepromising. This paper will review the cognitive
benefits associated with AE and focus on
aspects of cognition that are particularly
dependent hippocampal functioning such as
episodic memory formation (Figure1).

Alzheimer’s disease (AD) is an age-related,
progressive,
andirreversible
neurodegenerative disorder characterized bycognitive and memory impairment. In 2015, a
total of 44 million people throughout the world
were thought to have AD; it is estimated that
this figure will double by 20501). Therefore,
there is currently a particular need to develop
eﬀective strategies that alleviate cognitive
dysfunction. In late years, Aerobic exercise(AE)andlifestylehas
beenwidelyacknowledged for improving brain health. In
particular, AE has a potent impact on
37

JAHS 7 (2)REVIEW

It has been suggested that mental challenges
may protect against cognitive decline andpotentially against AD14). Computer courses
and psychoeducation have moderate beneficial
effects 15). Stimulation by cognitive activities
has been associated with an increase inneuronal density, which increases the brain
reserve and plasticity2).
The relation between caloric restriction andbrain motivation is important; many years ago,humans needed to obtain their food by killingwild animals, which often involved vigorous
exercise16). The possible mechanism may be
associated with SIRT1, a protein with
nicotinamide adenine dinucleotide-dependent
deacetylaseoradenosine
diphosphate-ribosyltransferase
activity17),
because it was reported to increase in p25 CK
mice with characteristics similar to AD. In
addition, SIRT1 stimulation by resveratrol
protects against neuronal death. SIRT1 levels
also increase with NADp in vitro, and SIRT
induces an increase in α-secretase and decreasein β-amyloid deposition in primary cultures in amouse model of AD18). The relationshipbetween hunger and neuroprotection wasdemonstrated using ghrelin in a mouse modelof AD; the results showed improved cognitionin the water maze test and a decrease inamyloid-β levels and inflammation19).

LifestyleLifestyle strategies include physical activity,
mental challenges, energy restriction, andsocialization as preventive factors for AD2).
Physical activity, such as aerobic exercise, wasassociated with a reduction in AD-related
deficits in a cohort study3). However, a different
result was obtained in small cases4). Exercise
was reported to enhance hippocampal
neurogenesis5,6) and learning in aging rodents7).
There are three mechanisms proposed to
explain the neuroprotective effect of exercise.
(1) The release of neurotrophic factors such as
brain-derived neurotrophic factor (BDNF),
insulin-like growth factor (IGF-1), nerve
growth factor (NGF), and vascular endothelial
growth factor (VEGF)8,9) from neurons during
synaptic
activity,which
stimulateneurogenesis and synaptic neural plasticity
through the stimulation of the cAMP response
element-binding protein (CREB) transcription
factor.
(2) The reduction in free radicals in the
hippocampus, as well as the increase insuperoxide dismutase and endothelial nitricoxide synthase9).
(3) Peripheral signals that help to support thedemands of active neuronal networks, such as
BDNF release, in addition to energy
restriction in the brain10-13).

Figure1.

Chart of References Number

38

JAHS 7 (2)Socialization is important in mental andphysical development. A lack of socializationinduces loneliness, which has been associatedwith various diseases such as depression,
alcohol abuse, obesity, diabetes, hypertension,AD, and cancer20).

whereas others have suggested AE had no
significant impact on cognition at all38, 40-43).
Such inconsistencies may partially be
explained by the methodological variation
between RCTs, making it difficult tosystematically compare their findings inmeta-analyses43, 44). The exact nature of how
AE affects cognition is not yet clear.

Aerobic Exercise
The attention paid to how AE influences
cognitive performance has exploded in the past
decade. AE generally refers to exercise that
improves the efficiency of aerobic energy
producing systems by increasing maximal
oxygenuptakeandcardiorespiratory
endurance21).
Large-scale
epidemiologicalstudies have consistently correlated high levels
of aerobic fitness with greater academic
achievement and IQ scores22-24). However, in
addition to greater preservation of cognitive
function in old age25-28) and fewer incidences ofdementia29), this capacity to promote cognitive
performance implies that AE may have an
important clinical relevance in counteracting
the cognitive decline associated with aging ordementia30); this implication has catalyzed
attempts for systematic investigation. Many
randomized controlled trials (RCTs) haverecently been conducted using moderateintensity AE interventions (such as 30 min of
Nordic walking) that generally span 3–12
months and are mostly conducted in older
adults. Meta-analyses have found AE
interventions to improve cognitive performanceacross a variety of domains, including attention,
executive functioning, processing speed, motor
functioning, and memory in healthy young andmiddle aged adults31 -35); notably, this effect isobserved predominantly in older age groups31,
32, 36-38) as well as in older individuals with mild
cognitive impairments or dementia38-40).
The available evidence strongly suggests thatAE has a positive influence on cognition in
individuals of all age groups, particularly inolder adults. Some RCTs have stipulated that
AE influences divergent cognitive domains,

A Hippocam pus-Centric Approach
Several meta-analyses have denoted thetendency for RCTs to report improvements inmemory-based task performance following an
AE-based intervention32, 34, 38, 45).
The human hippocampus plays a vital role in
the formation of declarative memories, mostprominently in the formation of episodic andspatiotemporal memories46). Episodic memoryrefers to the recollection of autobiographicalevents and is related to spatial memory, whichrefers to one’s environment and spatial
orientation. Spatial and episodic memory
processes are inherently related given their
specific reliance on the hippocampus47) and thefact that episodic memories are encoded in a
spatiotemporal context48), making spatial
information important in episodic memory
formation. Furthermore, the hippocampus,
particularly the dentate gyrus (DG), is crucial
in selecting and separating similar events inspace and time, and hence pattern separation
is a main function attributed to the
hippocampus49-51). It is important to note thatgiven the requirement of a conscious experienceto form an episodic memory, at present episodic
memory cannot be directly studied in animals
given the lack of behavioral markers for theirconscious experience52). Contextual memory is
a process strongly related to episodic memorythat is also highly dependent on the
hippocampus and refers to the capacity for an
animal to make associations with salient
landmark objects and their environmental
context53). As there is currently no objective
proxy for studying episodic-like memory
39

JAHS 7 (2)LIMITATIONS

processinginanimals54),
hippocampal
functioning shall be considered here as afunction of contextual and spatial memory task
performance when referring to animal
literature and as a function of episodic andspatial memory task performance when
discussing human literature. Some humanstudies have focused on assessing the influenceof AE on hippocampus-dependent cognition andshown in older adults that AE was associatedwithimproved
performanceinboth
episodic55-59) and spatial60-62) memory tasks, aswell as in pattern separation tasks in young
adults63). Moreover, some studies havedemonstrated in preadolescent children andyoung adults that AE is selectively associatedwith improved performance in contextual64-66)
and spatial67, 68) memory tasks and not with lesshippocampus-dependent
tasks
such
as
attention, verbal memory, or item recognition.
We will then discuss both animal and humanstudies, which indicate that these structuralchanges may be driven by a cascade of
micro-scale neuroplastic mechanisms within
the hippocampus stimulated by AE. Despite alimited selection of studies, these findings
indicate that AE may have a positive influenceon hippocampus-dependent forms of cognitionin healthy human participants, similar to what
has been consistently shown in animal models.
Pertaining to its highly neuroplastic nature69),
the hippocampus is particularly vulnerable tostructural and functional deterioration in awide range of neurological and psychiatricdisorders70). The aforementioned studies
demonstrate that AE could have a positive
influence on hippocampal functioning, but asignificantly greater cohort of systematicinvestigations using human participants will
be necessary to outline this relationship on abroader cognitive level. A growing body ofevidence is also accumulating to suggest that
AE may have a prominent impact on
hippocampal structure in humans, as well as inanimal models.

Another issue in the conceptualization of
AE-based treatments is the lack of consensus
as to what type, intensity, or length of exercise
sessions has the strongest impact on the brain.
For example, some studies argue thathigh-intensity exercise is optimal for reducing
symptoms in MDD 71), while others havesuggested that that a mild 72) or a moderateintensity exercise intervention would be
optimal73). It is possible that exercise
intensities may vary depending on the purposeof the intervention. For example, it has beensuggestedthat
improvingcognitive
performance may require high-intensity,interval training but preserving cognitive
function in an aging brain may require a lower
intensity, more continuous protocol74). Exercise
type may also be an important factor. Althoughmost of the current literature has focused on
AE, other forms of exercise such as yoga 75) or
weight training76) may also be beneficial inpromoting brain health and cognition. Given
the growing interest in exercise as atherapeutic intervention, it is surprising thatvery few studies have attempted a systematic
evaluation for the most effective approach inpsychiatric populations77-80). It is importantthat future research is concentrated on
establishing the merits of different forms of
exercise and on detailed elucidation of thedose-response
relationshipbetweentheintensity and length of AE intervention andtherapeutic outcomes in different psychiatricpopulations.

CONCLUSION
There is, currently, a particular need todevelop effective strategies that alleviatecognitive dysfunction. Targeting deficits in theneuroplasticity of areas crucial to cognition,such as the hippocampus, is a promising
approach to remediating cognitive dysfunction.
AE interventions represent an effective method
for promoting hippocampal neuroplasticity and40

JAHS 7 (2)function, which encompasses few risks andseveral additional benefits for the patient.
Future research should be aimed to establish
standardized methodologies for investigating
AE and to determine the most effective method
for maximizing therapeutic outcomes with AE
intervention. Improving our understanding of
the role of lifestyle factors, such as exercise, inmaintaining and promoting brain function
could have major impact on the formulation oftreatment and preventive strategies forpsychiatricandneurologicaldisorders.
Research demonstrating the potential of AE inpromotinghippocampal
structuralandfunctional integrity is growing at an impressive
rate as more and more work is translated fromanimal models to humans.

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