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Older Adults with Diabetes Mellitus Recent Advances in Geriatric Medicine, Vol. 1 69
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Recent Advances in Geriatric Medicine, 2016, Vol. 1, 73-91 73
CHAPTER 5
Halting the Decline in Cognition: New Insights into
Alzheimer’s Disease
Kareeann Sok Fun Khow
1,*
, Tuck Yean Yong
2
1
Aged and Extended Care Services, The Queen Elizabeth Hospital and Department of Medicine,
University of Adelaide, Adelaide, South Australia, Australia
2
Internal Medicine, Flinders Private Hospital, Adelaide, South Australia, Australia
Abstract: Alzheimer’s disease is a major public health concern globally and has been
identified as a research priority. Although this disease has been recognized for more
than a century, there is an urgent need to improve our understanding of its pathogenesis
in order to advance development of disease-modifying treatments. Clinical diagnosis of
Alzheimer’s disease remains the main method of identifying the disease but
neuroimaging and biomarkers are emerging as adjunct tests in selective cases. Only a
few pharmacological treatments are available for Alzheimer’s disease and modest
benefits are only observed in the mild-to-moderate disease. Without effective
treatment, non-pharmacological approaches and prevention remain important. Non-
pharmacological approaches such as exercise, cognitive stimulation therapy and
computerized mind games are potentially beneficial in slowing the progression of
Alzheimer’s disease. Behavioural and psychological symptoms in Alzheimer’s disease
are still challenging to manage and require a combination of non-pharmacological and
pharmacological approaches. Several novel therapies are currently under investigation
and clinical trials of these agents will reveal if they are beneficial in the treatment of
Alzheimer’s disease.
Keywords: Alzheimer’s disease, Anticholinesterase inhibitors, Behavioural
symptoms, Carers, Cognitive impairment, Dementia, Diagnosis, Lifestyle
modifications, Memantine, Psychological symptoms, Treatment.
*
Correspondence author Kareeann Sok Fun Khow: Aged and Extended Care Services, The Queen Elizabeth
Hospital, Woodville Road, Woodville South, South Australia 5011, Australia; Tel: +61 8 8222 6000; Fax: +61 8 8222
8593; E-mail: kareeann.khow@adelaide.edu.au.
Tuck Yean Yong (Ed)
All rights reserved-© 2016 Bentham Science Publishers
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74 Recent Advances in Geriatric Medicine, Vol. 1 Khow and Yong
INTRODUCTION
Alzheimer’s disease is the most frequent cause of dementia in many countries. It
was first named by Alois Alzheimer more than a century ago after examining a 51
year-old woman who was disoriented in time and place. He observed that “her
ability to retain information is impaired to the profoundest degree” [1].
Interestingly in 2013, this patient’s disease was finally understood when her DNA
was found to have a rare mutation in the presenilin 1 gene that causes early onset
Alzheimer’s disease [2].
Alzheimer’s disease has a significant impact on those with the condition as well
as family and caregivers. Progression of the disease leads to loss of functional
independence, the need for residential care and medical complications resulting in
deaths.
EPIDEMIOLOGY
The Delphi study estimated that there were about 24 million people worldwide
with dementia in 2001 and the majority are thought to have Alzheimer’s disease
[3]. It is predicted that the figure will rise to 42.3 million in 2020 and 81.1 million
by 2040.
In 2010, 35.6 million people were estimated to have lived with dementia
worldwide, with numbers predicted to increase two-fold every 20 years, to 65.7
million in 2030 and 115.4 million in 2050 [4]. In 2010, 58% of all people with
dementia lived in countries with low or middle incomes, with this proportion
anticipated to rise to 63% in 2030 and 71% in 2050.
RISK FACTORS
A consensus report from a panel of experts summarized some of the most
consistently identified risk factors in Alzheimer’s disease [5]. They found that
smoking, depression, diabetes mellitus, metabolic syndrome and the
apolipoprotein e4 (APOE e4) gene mutation were associated with increased risk
of cognitive decline. The most prevalent genetic risk factor for late onset disease
is the apolipoprotein ε4 allele, a gene for lipid transport in the brain. Over 65% of
people with Alzheimer’s disease are carriers of ε4 but only about 15% of the
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New Insights into Alzheimer’s Disease Recent Advances in Geriatric Medicine, Vol. 1 75
population possess it [6].
A family history of dementia is one of the most consistently reported risk factors
for Alzheimer’s disease [7]. Among patients with late-onset disease, first-degree
relatives have about a two-fold increase in their lifetime risk of the disease [7]. In
addition, the disease is more concordant in monozygotic twins than dizygotic
twins [8]. Apart from genetic factors, many treatable medical conditions are also
associated with an increased risk of Alzheimer’s disease, including stroke,
hypertension and hypercholesterolaemia [9 - 11].
PATHOGENESIS
There are three main hypotheses on the pathogenesis and aetiology of
Alzheimer’s disease: the amyloid plaques, neurofibrillary tangles and changes in
neurotransmitter levels such as acetylcholine.
The amyloid hypothesis proposes that the pathological formation of amyloid
plaques are directly toxic to cells and disrupt neurotransmission. These
extracellular plaques are mainly made up of insoluble fibrils of amyloid beta (Aβ)
peptide, which is formed when β-secretase and γ-secretase enzymes cleave
amyloid precursor protein (APP). The ε4 allele is thought to promote deposition
of Aβ [6]. However Aβ deposition does not correlate strongly with brain atrophy;
nor is it detected consistently in people with early Alzheimer’s-like
neurodegeneration [12].
“Hyperphosphorylated” tau has been hypothesized as the cause of neurofibrillary
tangles [13]. Tau, an insoluble protein, stabilises microtubules which in turn
maintain the axons connecting neurons to one another. Hyperphosphorylated tau
is thought to weaken axons because it does not bind to microtubules and it also
forms protein filaments, which lead to neurofibrillary tangles. Neurofibrillary
tangles correlate better with cognitive status and neuronal loss than the presence
of amyloid plaques [14].
The third hypothesis focuses on the neurotransmitter acetylcholine. In people with
Alzheimer’s disease, less acetylcholine is present in their brains compared to
those without dementia [15]. It is postulated that degeneration of the basal
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76 Recent Advances in Geriatric Medicine, Vol. 1 Khow and Yong
nucleus, the area of the brain that stimulates acetylcholine production and release,
is responsible for this reduction. Another neurotransmitter in cortical areas
involved in memory and learning is glutamate. In Alzheimer’s disease, excess
glutamate has been suggested to cause chronic activation of N-methyl-D-aspartate
(NMDA) receptors, resulting in intracellular calcium overload and neuronal death
from excitotoxicity [16].
DIAGNOSIS
Definite diagnosis of Alzheimer’s disease can currently be made only at post-
mortem. However, earlier diagnosis may be possible with new diagnostic
investigations and criteria. Clinically it is only possible to make a probable
diagnosis of the disease. This can be achieved by taking a thorough history of the
symptoms and temporal patterns from the patient and other sources such as
partner, carer or family members. Assessment is focused on determining the
presence and severity of cognitive impairment and the effects on social,
occupational and other instrumental functions. A neuropsychological assessment
may also be included.
Typically the initial symptom of Alzheimer’s disease involves an inability to
retain recently learned information but memory of remote events is relatively
spared until later. When the disease progresses, other cognitive areas such as
language, abstract reasoning, executive function or decision making are impaired
to varying degrees and this can lead to difficulty at work, social engagement or
household activities. Deterioration in memory is often associated with changes in
mood [17].
The Mini-Mental State Examination (MMSE) is one of the most commonly used
tests for cognition, which has good sensitivity and specificity for dementia, but
poor ability to recognize mild cognitive impairment [18, 19]. Using the MMSE,
one study found that 25% of patients admitted to subacute care had dementia
based on this test [20]. Among these, 70% were newly diagnosed after admission
to subacute care.
An operationalised clinical approach with criteria such as the NINCDS-ADRDA
(National Institute of Neurological and Communicative Disorders and Stroke and
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New Insights into Alzheimer’s Disease Recent Advances in Geriatric Medicine, Vol. 1 77
the Alzheimer’s Disease and Related Disorders Association) has relatively good
sensitivity (65%) and specificity (75%) for differentiating patients with probable
Alzheimer’s disease and those without dementia [21]. However its ability to
differentiate between Alzheimer’s disease and other forms of dementia is less
precise (23-88%) [21].
BEHAVIOURAL AND PSYCHOLOGICAL SYMPTOMS
Behavioural and psychological symptoms of dementia (BPSD) include
noncognitive symptoms and behaviours that commonly occur in patients with
dementia [22]. Clinically significant BPSD are found in about 30% of
community-dwelling people with dementia [23]. However this rises to almost
80% in people with dementia living in residential facilities [24]. BPSD symptoms
tend to fluctuate. Symptom clusters include mood disorders (depression, anxiety
and apathy/indifference), psychotic cluster (delusions and hallucinations),
aberrant motor behaviours (pacing, wandering and other purposeless behaviours)
and inappropriate behaviours (agitation, disinhibition and euphoria) [25]. The
estimated proportion of patients with dementia affected by BPSD is shown in
Table 1 [26 - 32]. BPSD are often associated with increased morbidity, increased
cost of caring for the patient and decrease in quality of life for both patients and
caregiver(s).
Table 1. Estimated proportion of patients with dementia affected by BPSD.
Symptom Proportion of Patients with Dementia References
Anxiety 24-65% [26]
Apathy 48-92% [26]
Delusions and hallucinations 9.2-36.0% [27]
Depression 33-50% [29, 30]
Disinhibition 36% [26]
Euphoria 3.5-8.0% [26, 33]
Irritability/mood lability/agitation 35-54% [26]
Sleep disturbances 25% [32]
Stereotyped behaviours (e.g., pacing, wandering) 12-84% [26]
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78 Recent Advances in Geriatric Medicine, Vol. 1 Khow and Yong
NEUROIMAGING
According to evidence-based recommendations, CT or MRI are indicated if
intracranial lesions or diseases that might cause or contribute to dementia
syndromes (such as tumour, subdural haematomas, hydrocephalus or
cerebrovascular disease) are clinically suspected [21].
Semi-quantitative structural MRI has been used to identify changes in medial
temporal lobe atrophy between patients with Alzheimer’s disease and age-
matched control, with moderately high sensitivity and specificity of greater than
85% [21]. Furthermore, medial temporal atrophy has been proposed as a feature
that can identify patients with mild cognitive impairment who will eventually
progress to Alzheimer’s disease. However, differences in medial temporal atrophy
do not distinguish between Alzheimer’s disease and non-Alzheimer’s dementias.
Positron emission tomography (PET) with fluorodeoxyglucose has been found to
have good accuracy in differentiating patients with probable Alzheimer’s disease
from both normal control people and those with non-Alzheimer’s disease
dementias [34]. A decrease of glucose metabolism in the temporal parietal regions
and in the posterior cingulated cortex are findings commonly described in
Alzheimer’s disease. A meta-analysis has reported sensitivity and specificity of
86% for diagnosis of Alzheimer’s disease with PET imaging but there were wide
variations between studies [34]. Lower diagnostic values were found when
distinguishing between Alzheimer’s disease and non-Alzheimer’s dementia [34].
A Cochrane systematic review analysed 14 studies evaluating the diagnostic
accuracy of PET in determining the progression of mild cognitive impairment to
Alzheimer’s disease [35]. This review found that there was considerable
variability of specificity values of PET and defined thresholds for test positivity
was lacking and indicated that currently available evidence did not support the
routine use of this imaging in people with mild cognitive impairment.
The use of amyloid PET in Alzheimer’s disease was first reported in 2004 [36]. A
systematic review has found that amyloid PET had a sensitivity and specificity of
85% in differentiating Alzheimer’s disease from absence of the disorder [37].
However the specificity of this imaging approach was only 46-88% for
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