scholarly journals Intermittent Light Exposures in Humans: A Case for Dual Entrainment in the Treatment of Alzheimer's Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Mariana G. Figueiro ◽  
Sagan Leggett

Circadian sleep disorders are common among American adults and can become especially acute among older adults, especially those living with Alzheimer's disease (AD) and mild cognitive impairment (MCI), leading to the exacerbation of symptoms and contributing to the development and advancement of the diseases. This review explores the connections between circadian sleep disorders, cognition, and neurodegenerative disease, offering insights on rapidly developing therapeutic interventions employing intermittent light stimuli for improving sleep and cognition in persons with AD and MCI. Light therapy has the potential to affect sleep and cognition via at least two pathways: (1) a regular and robust light-dark pattern reaching the retina that promotes circadian phase shifting, which can promote entrainment and (2) 40 Hz flickering light that promotes gamma-wave entrainment. While this is a new area of research, preliminary evidence shows the potential of dual circadian and gamma-wave entrainment as an important therapy not only for those with AD, but for others with cognitive impairment.

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.


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.


2022 ◽  
Vol 12 ◽  
Author(s):  
Riccardo Cremascoli ◽  
Davide Sparasci ◽  
Gianluca Giusti ◽  
Stefania Cattaldo ◽  
Elisa Prina ◽  
...  

It is shown that the circadian system is affected in patients with Alzheimer’s disease (AD) even at an early stage of the disease and that such dysfunction may be detrimental to sleep, mood, and cognitive functioning. Light is a strong central modulator of the circadian rhythms and is potentially beneficial to mood and cognitive functioning via a direct effect or indirectly via its modulating effects on circadian rhythms. This study focuses on tracking the effect of light therapy on sleep quality, mood, and cognition in AD of mild/moderate severity. We performed a single-blind randomized controlled trial to investigate the effects of a light therapy treatment tailored to the individual circadian phase as measured by dim light melatonin onset (DLMO). Such a treatment induced an objective circadian phase shift consistent with the melatonin phase response curve to light exposure, led to a shortening of the phase angle DLMO-falling asleep time, and was associated with an improvement in subjective sleep quality and cognitive performance.


Author(s):  
Zara Melikyan ◽  
Heather Romero ◽  
Kathleen A. Welsh-Bohmer

Alzheimer’s disease (AD) is the most common cause of dementia in aging. Currently, therapeutic interventions are being initiated earlier in the disease course. The rationale of this strategy is to take advantage of the still healthy neuronal systems to optimize function, slow cognitive decline, and facilitate adaptive compensation in deficient brain networks. This chapter provides an overview and critique of the evidence supporting the enhancement of cognitive function at the early symptomatic stage of AD, so-called mild cognitive impairment due to AD (MCI-AD). It reviews the clinical diagnosis of MCI-AD, underscoring the differences between this condition and healthy brain aging and highlighting the importance of fluid and imaging biomarkers in ensuring reliable diagnosis and providing targets for therapeutic modification. Next, it discusses techniques to enhance cognition in MCI, with an emphasis on nonpharmacological interventional approaches. It concludes with a discussion of future challenges and opportunities in the treatment of MCI-AD.


1997 ◽  
Vol 170 (2) ◽  
pp. 156-158 ◽  
Author(s):  
Zuzana Walker ◽  
Ruth L. Allen ◽  
Sukhwinder Shergill ◽  
Cornelius L. E. Katona

BackgroundLewy body dementia (LBD) is emerging as a common cause of degenerative dementia. However, LBD cannot yet be diagnosed with certainty in life. There is some preliminary evidence that the pattern of cognitive impairment in LBD is different from that in Alzheimer's disease (AD). We set out to compare the performance on different subtests of the Cambridge Cognitive Examination (CAMCOG) of LBD patients and AD patients who were similar in overall degree of cognitive impairment.MethodsAll patients were recruited from a memory clinic LBD (n = 17) was diagnosed according to the McKeith clinical criteria. AD (n = 17) was diagnosed according to NINCDS-ADRDA criteria. The performances of LBD and AD patients on the neuropsychological subscales of the CAMCOG were compared by applying Hotelling's multivariate test of significance and subsequent univariate F tests.ResultsThere were no statistically significant differences between the two groups on Mini-Mental State Examination and global CAMCOG rating. Hotelling's test with LBD and AD as the between-group factor and the neuropsychological subtests from CAMCOG as dependent variables revealed a statistically significant group effect (P < 0.05). Univariate F tests showed that recall (P < 0.02) and praxis (P < 0.003) significantly contributed to this effect.ConclusionsThese results suggest that there may be different neuropsychological profiles in the two conditions, with LBD subjects being better on recall but worse on praxis than those with AD.


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