12 Aptamers for the Diagnosis and Therapy …
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in recent years, especially in the field of diagnosis and therapy. Aptamers, due to their
advantages, could be used to develop new approaches for the diagnosis or therapy
of these neurodegenerative diseases. This chapter aims to provide an update on the
applications of aptamers in the field of diagnosis and therapy of neurodegenerative
diseases.
12.2 The Applications of Aptamers in Neurodegenerative
Diseases
Neurodegenerative disorders have attracted worldwide attention because of the prevalent incidence in the upcoming aging society [33]. These diseases are characterized
by neuronal dysfunction and death, and most of these diseases are associated with
the accumulation of misfolded proteins [34], such as amyloid β-protein(Aβ), tau,
alpha-synuclein (α-syn), prion protein (PrP), and huntingtin protein (HTT) [31, 32,
35, 36]. Therefore, detecting these misfolded proteins would be potential ways to
diagnose these diseases, and slowing down or preventing neuronal dysfunction and
death would be potential approaches to treat these diseases. Aptamers could bind
with these target proteins, and most of them could also prevent these protein aggregation process or decrease the negative effects of these misfolded proteins, which
suggests aptamers might be novel agents not only in the diagnosis but also in the
therapy of these diseases.
12.2.1 The Applications of Aptamers in AD
With the great increase of the human life span in the world, AD, one of the major
diseases of progressive neurodegenerative diseases, is becoming a heavy burden and
challenge in most countries [37–39]. AD is characterized by the presence of insoluble plaques and tangles composed of Aβ and phosphorylated tau (p-tau) protein,
which is followed by progressive functional disruption of neuronal networks. There
are various descriptive hypotheses regarding the causes of AD, but the amyloid
hypothesis and tau propagation hypotheses attract the attention of scientists all over
the world. The amyloid hypothesis proposes that AD is characterized by aggregates
of neuritic plaques composed primarily of the 42 and 40 amino acid Aβ peptides,
which could trigger a cascade of neurobiological events and other neuronal changes
[40, 41]. The tau hypothesis suggests that the ultimate causative factor of AD is the
tangling and deposition of p-tau protein. These p-tau proteins are prone to aggregation
resulting in nerve fiber entanglement and feature various deficiencies in physiological functions [42–44]. Although currently there is no treatment known to reverse or
delay the progression of this disease, Aβ and tau have been the targets for diagnosis
and therapy of AD.
353
in recent years, especially in the field of diagnosis and therapy. Aptamers, due to their
advantages, could be used to develop new approaches for the diagnosis or therapy
of these neurodegenerative diseases. This chapter aims to provide an update on the
applications of aptamers in the field of diagnosis and therapy of neurodegenerative
diseases.
12.2 The Applications of Aptamers in Neurodegenerative
Diseases
Neurodegenerative disorders have attracted worldwide attention because of the prevalent incidence in the upcoming aging society [33]. These diseases are characterized
by neuronal dysfunction and death, and most of these diseases are associated with
the accumulation of misfolded proteins [34], such as amyloid β-protein(Aβ), tau,
alpha-synuclein (α-syn), prion protein (PrP), and huntingtin protein (HTT) [31, 32,
35, 36]. Therefore, detecting these misfolded proteins would be potential ways to
diagnose these diseases, and slowing down or preventing neuronal dysfunction and
death would be potential approaches to treat these diseases. Aptamers could bind
with these target proteins, and most of them could also prevent these protein aggregation process or decrease the negative effects of these misfolded proteins, which
suggests aptamers might be novel agents not only in the diagnosis but also in the
therapy of these diseases.
12.2.1 The Applications of Aptamers in AD
With the great increase of the human life span in the world, AD, one of the major
diseases of progressive neurodegenerative diseases, is becoming a heavy burden and
challenge in most countries [37–39]. AD is characterized by the presence of insoluble plaques and tangles composed of Aβ and phosphorylated tau (p-tau) protein,
which is followed by progressive functional disruption of neuronal networks. There
are various descriptive hypotheses regarding the causes of AD, but the amyloid
hypothesis and tau propagation hypotheses attract the attention of scientists all over
the world. The amyloid hypothesis proposes that AD is characterized by aggregates
of neuritic plaques composed primarily of the 42 and 40 amino acid Aβ peptides,
which could trigger a cascade of neurobiological events and other neuronal changes
[40, 41]. The tau hypothesis suggests that the ultimate causative factor of AD is the
tangling and deposition of p-tau protein. These p-tau proteins are prone to aggregation
resulting in nerve fiber entanglement and feature various deficiencies in physiological functions [42–44]. Although currently there is no treatment known to reverse or
delay the progression of this disease, Aβ and tau have been the targets for diagnosis
and therapy of AD.