Paranoid delusions and hallucinations and bright light therapy in Alzheimer's disease

2002 ◽  
Vol 17 (11) ◽  
pp. 1071-1072 ◽  
Author(s):  
Shird Dieter Schindler ◽  
André Graf ◽  
Peter Fischer ◽  
Anton Tölk ◽  
Siegfried Kasper
2020 ◽  
Vol 77 (1) ◽  
pp. 113-125 ◽  
Author(s):  
Ilaria Roccaro ◽  
Daniela Smirni

Background: A system of photosensitive retinal ganglion cells provides ‘non-visual’ information on the circadian sequences of light to the suprachiasmatic nucleus (SCN), which, as the ‘master clock’, synchronizes the chronobiological mechanisms of all the biological clocks. Damage to SCN structure alters circadian behavioral and hormonal rhythms and interferes with a regular sleep-wake pattern. Several studies have shown that, in aging and in Alzheimer’s disease (AD), circadian rhythms change their synchronization with the environment and behavior loses sync with light. Objective: The current overview aims to examine research studies showing the effect of bright light therapy (BLT) on sleep disorders and sleep-wake patterns in AD. Methods: A literature search was conducted, taking into consideration the relevant studies over the last 20 years. Fifteen studies have been thorough: seven followed an environmental-architectural approach and eight followed a treatment devices approach. Results: Studies agree in considering BLT as a promising non-pharmacological intervention to compensate for circadian rhythm alterations and they support the need for standardized protocols that allow a comparison between multicenter studies. Conclusion: Interestingly, in an attempt to contain the spread of the COVID-19 pandemic, health authorities have forced the population to stay home. Therefore, AD people are not currently able to enjoy exposure to sunlight. It is predictable that they may experience an exacerbation of circadian disturbances and that the BLT can be an effective response to prevent such exacerbation.


Author(s):  
A. H. M. Safayet Ullah Prodhan ◽  
Cinzia Cavestro ◽  
Mohammad Amjad Kamal ◽  
Md Asiful Islam

: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by sleep, behavioral, memory, and cognitive deteriorations. Sleep disturbance (SD) is a major disease burden in AD which has a reciprocal relationship with AD pathophysiology. It aggravates memory, behavioral, and cognitive complications in AD. Different studies found that melatonin hormone levels reduce even in the pre-clinical stages of AD. Melatonin is the primary sleep-regulating hormone and a potent antioxidant with neuroprotective roles. The decrease in melatonin levels can thus promote SD and AD neuropathology. Exogenous melatonin has the potential to alleviate neuropathology and SD in AD by different mechanisms. Various studies have been conducted so far that assessed the efficacy of exogenous melatonin to treat SD in AD. Though most of the studies suggest that melatonin is useful to ameliorate SD in AD, the remaining studies show opposite results. The timing, dosage, and duration of melatonin administration along with disease condition, genetic, environmental, and some other factors can be responsible for the discrepancies between the studies. More extensive trials with longer durations and higher dosage forms and studies including bright light therapy and melatonin agonists (ramelteon, agomelatine, and tasimelteon) should be performed to determine the efficacy of melatonin to treat SD in AD.


2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Dawit A. Weldemichael ◽  
George T. Grossberg

Circadian Rhythm Disturbances (CRDs) affect as many as a quarter of Alzheimer's disease (AD) patients during some stage of their illness. Alterations in the suprachiasmatic nucleus and melatonin secretion are the major factors linked with the cause of CRDs. As a result, the normal physiology of sleep, the biological clock, and core body temperature are affected. This paper systematically discusses some of the causative factors, typical symptoms, and treatment options for CRDs in patients with AD. This paper also emphasizes the implementation of behavioral and environmental therapies before embarking on medications to treat CRDs. Pharmacotherapeutic options are summarized to provide symptomatic benefits for the patient and relieve stress on their families and professional care providers. As of today, there are few studies relative to CRDs in AD. Large randomized trials are warranted to evaluate the effects of treatments such as bright light therapy and engaging activities in the reduction of CRDs in AD patients.


2020 ◽  
Vol 19 (2) ◽  
pp. 248-264 ◽  
Author(s):  
Ashish Sharma ◽  
Gautam Sethi ◽  
Murtaza M. Tambuwala ◽  
Alaa A. A. Aljabali ◽  
Dinesh Kumar Chellappan ◽  
...  

: All mammalian cells exhibit circadian rhythm in cellular metabolism and energetics. Autonomous cellular clocks are modulated by various pathways that are essential for robust time keeping. In addition to the canonical transcriptional translational feedback loop, several new pathways of circadian timekeeping - non-transcriptional oscillations, post-translational modifications, epigenetics and cellular signaling in the circadian clock - have been identified. The physiology of circadian rhythm is expansive, and its link to the neurodegeneration is multifactorial. Circadian rhythm disruption is prevelant in contamporary society where light-noise, shift-work, and transmeridian travel are commonplace, and is also reported from the early stages of Alzheimer's disease (AD). Circadian alignment by bright light therapy in conjunction with chronobiotics is beneficial for treating sundowning syndrome and other cognitive symptoms in advanced AD patients. We performed a comprehensive analysis of the clinical and translational reports to review the physiology of the circadian clock, delineate its dysfunction in AD, and unravel the dynamics of the vicious cycle between two pathologies. The review delineates the role of putative targets like clock proteins PER, CLOCK, BMAL1, ROR, and clock-controlled proteins like AVP, SIRT1, FOXO, and PK2 towards future approaches for management of AD. Furthermore, the role of circadian rhythm disruption in aging is delineated.


Author(s):  
Sarah Bogen ◽  
Tanja Legenbauer ◽  
Stephanie Gest ◽  
Martin Holtmann

Abstract. Objective: In recent years, bright light therapy (BLT) has been used to treat depression and to stabilize circadian rhythms. In this study we evaluated whether it is also helpful for comorbid symptoms of affective and behavioral dysregulation in depressive inpatients. Method: This article reports a secondary analysis comparing two subgroups of depressive participants with comorbid affective and behavioral dysregulation, captured with the dysregulation-profile of the Strengths and Difficulties Questionnaire (SDQ-DP; n = 16 vs. n = 11). Participants were randomly allocated to active BLT (10,000 lux) or control BLT (approx. 100 lux), and received 45 minutes of BLT for 2 weeks. SDQ-DP scores, sleep parameters, and circadian preference were assessed at baseline, after the intervention, and 3 weeks later. Results: No direct effects on SDQ-DP scores were observed. Sleep improved in both conditions. Only in the active BLT condition was a circadian phase advance found. Correlation and regression analyses indicated an indirect, circadian effect for improved SDQ-DP scores. Conclusions: The data of this pilot trial should be considered preliminary and merely descriptive. Further research is warranted.



Author(s):  
Zeba Mueed ◽  
Pankaj Kumar Rai ◽  
Mohammad A. Kamal ◽  
Nitesh Kumar Poddar

Alzheimer’s disease (AD), characterized by abnormally phosphorylated tau, paired helical filaments (PHFs), neurofibrillary tangles (NFTs), deregulated mammalian target of rapamycin (mTOR), Aβ deposits, is a multifactorial disease with sleep disorders being one of the causative agents. Therefore, we have reviewed the literature and have tried to decode the existence of positive feedback, reciprocal and a bidirectional relationship allying between sleep disturbances and AD. Much light has been thrown on the role of tau pathology and amyloid pathology in sleep pathology and its association with AD pathology. We have also discussed the role of melatonin in regulating sleep disorders and AD. The neuroprotective action of melatonin via inhibiting tau hyperphosphorylation and Aβ deposition has also been pondered upon. Moreover, astrocytes involvement in aggravating AD has also been highlighted in this review. Several therapeutic approaches aimed at improving both sleep disorders and AD have been duly discussed such as administration of antidepressants and antihistamines, immunotherapy, metal chelators, melatonin supplementation, light therapy and physical activity. Despite consistent efforts, the complete etiology concerning sleep disorder and AD is still unclear. Therefore, further research is needed to unravel the mechanism involved and also to develop strategies that may help in obstructing AD in its preclinical stage.


Neurology ◽  
2019 ◽  
pp. 10.1212/WNL.0000000000007090 ◽  
Author(s):  
Sonja Rutten ◽  
Chris Vriend ◽  
Jan H. Smit ◽  
Henk W. Berendse ◽  
Eus J.W. van Someren ◽  
...  

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