Circadian and sleep dysfunction in Alzheimer’s disease

Uddin, Md. Sahab; Tewari, Devesh; Mamun, Abdullah Al; Kabir, Md. Tanvir; Niaz, Kamal; Wahed, Mir Imam Ibne; Barreto, George E.; Ashraf, Ghulam Md

doi:10.1016/j.arr.2020.101046

Cited by 115 publications

(61 citation statements)

References 211 publications

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“…Maintaining a normal circadian rhythm is essential in order to optimize quality of life and preserve health. Sleep-wake disturbances are common secondary symptoms of AD that have been observed in studies on patients with AD (Uddin et al, 2020) and on the 3×Tg and 5×FAD mouse models of AD (Sterniczuk et al, 2010;Sethi et al, 2015). Moreover, the pineal gland, which adjusts sleep patterns by producing melatonin, and the SCN, which is involved in the regulation and production of biological rhythms, are vulnerable regions in AD (Buijs and Kalsbeek, 2001;Wu and Swaab, 2005;Roy et al, 2019).…”

Section: The Role Of Ghrelin In Ad-related Sleep-wake Disturbancesmentioning

confidence: 99%

The Potential Roles of Ghrelin in Metabolic Syndrome and Secondary Symptoms of Alzheimer’s Disease

Kim¹,

Nam²,

Shin³

et al. 2020

Front. Neurosci.

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Although the major causative factors of Alzheimer's disease (AD) are the accumulation of amyloid β and hyperphosphorylated tau, AD can also be caused by metabolic dysfunction. The major clinical symptom of AD is cognitive dysfunction. However, AD is also accompanied by various secondary symptoms such as depression, sleep-wake disturbances, and abnormal eating behaviors. Interestingly, the orexigenic hormone ghrelin has been suggested to have beneficial effects on AD-related metabolic syndrome and secondary symptoms. Ghrelin improves lipid distribution and alters insulin sensitivity, effects that are hypothesized to delay the progression of AD. Furthermore, ghrelin can relieve depression by enhancing the secretion of hormones such as serotonin, noradrenaline, and orexin. Moreover, ghrelin can upregulate the expression of neurotrophic factors such as brain-derived neurotrophic factor and modulate the release of proinflammatory cytokines such as tumor necrosis factor α and interleukin 1β. Ghrelin alleviates sleep-wake disturbances by increasing the levels of melatonin, melanin-concentrating hormone. Ghrelin reduces the risk of abnormal eating behaviors by increasing neuropeptide Y and γ-aminobutyric acid. In addition, ghrelin increases food intake by inhibiting fatty acid biosynthesis. However, despite the numerous studies on the role of ghrelin in the AD-related pathology and metabolic disorders, there are only a few studies that investigate the effects of ghrelin on secondary symptoms associated with AD. In this mini review, our purpose is to provide the insights of future study by organizing the previous studies for the role of ghrelin in AD-related pathology and metabolic disorders.

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Section: The Role Of Ghrelin In Ad-related Sleep-wake Disturbancesmentioning

confidence: 99%

The Potential Roles of Ghrelin in Metabolic Syndrome and Secondary Symptoms of Alzheimer’s Disease

Kim¹,

Nam²,

Shin³

et al. 2020

Front. Neurosci.

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“…Neuropathological alterations that take place in dementia patients are accountable for changes in the perception of pain ( Van Kooten et al., 2016 ). Though these changes can be common in different forms of dementia, however, scientists are trying to investigate the pain perception and processing in the patients of Alzheimer’s disease (AD), which is characterized by behavioral and cognitive impairments ( Al Mamun et al., 2020b ; Uddin et al., 2020a ; Uddin et al., 2020l ). Neuropathological hallmarks of AD are extracellular accumulations of amyloid beta (Aβ) as well as intracellular accumulations of neurofibrillary tangles (NFTs) that are comprised of hyperphosphorylation of tau ( Uddin et al., 2019 ; Mamun et al., 2020 ; Uddin et al., 2020d ).…”

Section: Introductionmentioning

confidence: 99%

Emerging Promise of Cannabinoids for the Management of Pain and Associated Neuropathological Alterations in Alzheimer’s Disease

et al. 2020

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Alzheimer's disease (AD) is an irreversible chronic neurodegenerative disorder that occurs when neurons in the brain degenerate and die. Pain frequently arises in older patients with neurodegenerative diseases including AD. However, the presence of pain in older people is usually overlooked with cognitive dysfunctions. Most of the times dementia patients experience moderate to severe pain but the development of severe cognitive dysfunctions tremendously affects their capability to express the presence of pain. Currently, there are no effective treatments against AD that emphasize the necessity for increasing research to develop novel drugs for treating or preventing the disease process. Furthermore, the prospective therapeutic use of cannabinoids in AD has been studied for the past few years. In this regard, targeting the endocannabinoid system has considered as a probable therapeutic strategy to control several associated pathological pathways, such as mitochondrial dysfunction, excitotoxicity, oxidative stress, and neuroinflammation for the management of AD. In this review, we focus on recent studies about the role of cannabinoids for the treatment of pain and related neuropathological changes in AD.

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“…People who inherit one copy of the APOE4 allele may cause a higher risk of raising AD, and people who possess two copies of the APOE4 allele are at greater risk of progressing AD [21,22]. The APOE4 gene may also be accompanied by an earlier onset of memory dysfunction and other symptoms in comparison with AD patients who do not have this gene.…”

Section: Introductionmentioning

confidence: 99%

Molecular Insight into the Therapeutic Promise of TargetingAPOE4for Alzheimer’s Disease

Mamun

Uddin

Bashar

et al. 2020

Oxidative Medicine and Cellular Longevity

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease that causes chronic cognitive dysfunction. Most of the AD cases are late onset, and the apolipoprotein E (APOE) isoform is a key genetic risk factor. The APOE gene has 3 key alleles in humans including APOE2, APOE3, and APOE4. Among them, APOE4 is the most potent genetic risk factor for late-onset AD (LOAD), while APOE2 has a defensive effect. Research data suggest that APOE4 leads to the pathogenesis of AD through various processes such as accelerated beta-amyloid aggregations that raised neurofibrillary tangle formation, cerebrovascular diseases, aggravated neuroinflammation, and synaptic loss. However, the precise mode of actions regarding in what way APOE4 leads to AD pathology remains unclear. Since APOE contributes to several pathological pathways of AD, targeting APOE4 might serve as a promising strategy for the development of novel drugs to combat AD. In this review, we focus on the recent studies about APOE4-targeted therapeutic strategies that have been advanced in animal models and are being prepared for use in humans for the management of AD.

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Circadian and sleep dysfunction in Alzheimer’s disease

Cited by 115 publications

References 211 publications

The Potential Roles of Ghrelin in Metabolic Syndrome and Secondary Symptoms of Alzheimer’s Disease

The Potential Roles of Ghrelin in Metabolic Syndrome and Secondary Symptoms of Alzheimer’s Disease

Emerging Promise of Cannabinoids for the Management of Pain and Associated Neuropathological Alterations in Alzheimer’s Disease

Molecular Insight into the Therapeutic Promise of TargetingAPOE4for Alzheimer’s Disease

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