Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • The relationship between AG and tau

    2022-11-11

    The relationship between AG and tau deposition in the presence of Aβ burden warrants more research in AD and in other primary tauopathies (not associated with accumulation of Aβ plaques). Our findings highlight the importance of measuring AG, as this relationship was not evident for total CH5138303 use (CMRGlc) alone. One possible explanation for the relationship between AG and tau deposition is that tau, among its various toxic effects (Shi et al., 2017), might impair processes that demand AG, such as synaptic plasticity. Alternatively, AG loss could potentially accelerate tauopathy. Our findings suggest that longitudinal studies of AG and AD pathology will help to further define this relationship.
    Disclosure statement
    Acknowledgements
    Introduction Alzheimer’s disease (AD) is the most common form of dementia, accounting for up to 60% of cases (Rizzi et al., 2014) and agitation is a common neuropsychiatric syndrome that affects around 50% of patients with AD (Aalten et al., 2005; Burns et al., 1990; Lyketsos et al., 2000). Agitation covers a broad range of symptoms including anxiety and irritability, motor restlessness and abnormal vocalization, as well as observable behaviors such as pacing, wandering, aggression, shouting and night-time disturbance (Howard et al., 2001). A recent consensus definition of agitation in dementia characterized the syndrome as observed or inferred evidence of emotional distress associated with excessive motor activity, verbal or physical aggression (Cummings et al., 2015) (Table 1). Agitation significantly reduces quality of life for patients and caregivers, precipitates earlier institutionalisation (Okura et al., 2011), and is associated with more rapid disease progression and earlier death (Peters et al., 2015). Although non-pharmacological approaches to the treatment of agitation have shown some evidence of efficacy in a care home setting (Livingston et al., 2014), patients who exhibit more severe agitation with higher levels of distress and associated risk often require additional treatment with medication. However, there are no safe and effective drug treatments for agitation, as the best evidence is for short-term use of atypical antipsychotic drugs, which have modest efficacy and are associated with significant harm (sedation, falls, parkinsonism, stroke) and increased mortality (Ballard and Howard, 2006; Schneider et al., 2006), particularly in those aged over 80 years (Howard et al., 2016). Citalopram, a selective serotonin reuptake inhibitor (SSRI) may also have a degree of efficacy but is associated with worsening cognitive function and cardiac side effects (Porsteinsson et al., 2014). Disruption of the dynamic balance between cholinergic and monoaminergic neurotransmission has been proposed to underlie the behavioral and psychological symptoms of dementia (BPSD) in AD (Lanari et al., 2006), and previous reviews have summarized the role of specific neurotransmitter systems such as serotonin (5-HT) (Lanctôt et al., 2001) and noradrenaline (NA) (Herrmann et al., 2004b). However, BPSD is a non-specific catch-all that includes a wide range of emotional responses and behaviors (including agitation, apathy, psychosis and depression), which are likely to have distinct neurochemical and neurobiological bases in the AD brain (Lanari et al., 2006). There is increasing evidence that agitation is caused by dysfunction in specific neuronal networks involved in cognitive control and emotion regulation (Rosenberg et al., 2015), functions known to be modulated by interacting neurotransmitter systems (Del Arco and Mora, 2009). It is therefore logical as well as imperative that we should seek to understand the neurochemical basis of agitation in AD in order to effectively target treatment strategies. This paper aims to provide an up-to-date systematic review of the characteristics, methodology and findings of studies that have investigated the neurochemistry of agitation in AD. The recently established consensus definition of agitation (Cummings et al., 2015) will be used in the search criteria to optimize cross-study comparison, and the validity of reviewed studies will be discussed.