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- Itzhaki, Ruth F., et al.
(författare)
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Microbes and Alzheimer's Disease
- 2016
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Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 51:4, s. 979-984
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD [1–4]. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood [7]. The first observations of HSV1 in AD brain were reported almost three decades ago [8]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease [9, 10]. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic
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- Itzhaki, Ruth F., et al.
(författare)
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Microbes and Alzheimer's disease
- 2017
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Ingår i: Handbook of infection and Alzheimer's disease. - : IOS Press. - 9781614997054 - 9781614997061 ; , s. 3-8
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Bokkapitel (refereegranskat)
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- Schwarz, Johanna F. A., et al.
(författare)
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Shortened night sleep impairs facial responsiveness to emotional stimuli
- 2013
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Ingår i: Biological Psychology. - : Elsevier BV. - 0301-0511 .- 1873-6246. ; 93:1, s. 41-44
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Tidskriftsartikel (refereegranskat)abstract
- Sleep deprivation deteriorates mood, impairs the recognition of facial expressions, and affects the ability to regulate emotions. The present study investigated the effect of partial sleep deprivation on facial responses to emotional stimuli. Thirty-three healthy undergraduates were tested twice: after a night with (i) 8h and (ii) 4h sleep. Self-reported sleepiness and sustained attention (Psychomotor Vigilance Task) were assessed. Emotional reactivity was measured with facial Electromyogram (EMG) while participants were asked to respond with either compatible or incompatible facial muscles to emotional stimuli in order to study whether partial sleep deprivation caused slower reactions mainly in response to incompatible stimuli (due to an additional effort to suppress the compatible reaction caused by decreased inhibitory control) or in response to both compatible and incompatible stimuli. Self-reported sleepiness and reaction times in a sustained attention task significantly increased after one night of partial sleep deprivation. Facial reactions to emotional stimuli were decelerated. No significant interaction between sleep restriction and compatibility of the muscle to the picture valence could be observed. Hence, volitional facial reactions in response to emotional stimuli were slower after one night of reduced sleep, but affective inhibitory control was not significantly impaired. However, slowed facial responding to emotional stimuli may affect social interaction after sleep restriction.
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