Volume 24, Issue 6

In recent years, researchers have embarked on a search of computer-aided methods for diagnosis of the Alzheimer’s disease (AD) to help clinicians make the diagnosis earlier and more accurately such that treatment of the disease can begin sooner when there is a higher chance of success in slowing down the progression of this disease. This article presents a review of journal articles on brain signal- and image-based diagnosis of AD published in the past few years. The areas of signal processing, electroencephalogram and magnetoencephalogram are considered. In the area of image analysis, the following modalities are reviewed: magnetic resonance imaging (MRI), functional MRI, diffusion tensor MRI, and structural MRI. Computer-aided early diagnosis of the AD would be a major breakthrough with a very significant worldwide impact because medications would be able to slow down the progression of the disease. This review shows that this is a very active area in the frontier of brain research, with many multidisciplinary researchers exploring a variety of approaches using various types of brain signals and imaging technologies. The brain signal-based approaches will be able to point toward early onset diagnosis of the AD, but as the disease progresses, a multimodal approach can increase the accuracy of the diagnosis.

If an organism’s responding to its present location or more abstract situation is similar to its responding to discrete motivationally salient stimuli, then principles of stimulus-response relationships and their acquisition may apply to the organization of behavior that appears to be sensitive and appropriate to the organism’s external context. Locations or situations become motivationally salient, insofar as they acquire the ability to compel the organism to obtain a specific type of reward through more or less constrained exploratory or foraging behavior. The ventral hippocampus is proposed to play a key role in linking a salient situation or location with an appropriate mode of behavior, whereas allocentric information predicted and updated by the dorsal hippocampus may be associated with, or translated into, a sequence of orienting and locomotor actions. The impact of ventral hippocampal representations of salient situations on behavior is mediated by the ventral subiculum, ventromedial prefrontal cortex, and ventral striatum. Projecting via the ventral subiculum to the ventromedial prefrontal cortex and ventral striatum, the ventral hippocampus maps motivationally salient environmental information, as well as emotional information reflective of the internal physiological milieu, onto an instrumental or emotional behavior mode that represents a specialized, more or less purposeful, state of behavioral arousal and global locomotor activation.

Alzheimer’s disease (AD) is a complex neurodegenerative disorder, which involves many underlying pathological processes. Recently, it has been demonstrated that AD also includes impairments of insulin signaling in the brain. Type 2 diabetes is a risk factor for AD, and AD and diabetes share a number of pathologies. The classical hallmarks of AD are senile plaques and neurofibrillary tangles, which consist of amyloid-β and hyperphosphorylated tau. Based on the two hallmarks, transgenic animal models of AD have been developed, which express mutant human genes of amyloid precursor protein, presenilin-1/2, and tau. It is likely that these mouse models are too limited in their pathology. In this work, we describe mouse models that model diabetes and show insulin signaling impairment as well as neurodegenerative pathologies that are similar to those seen in the brains of AD patients. The combination of traditional AD mouse models with induced insulin impairments in the brain may be a more complete model of AD. Interestingly, AD mouse models treated with drugs that have been developed to cure type 2 diabetes have shown impressive outcomes. Based on these findings, several ongoing clinical trials are testing long lasting insulin analogues or GLP-1 mimetics in patients with AD.

Fatigue is defined as a condition or phenomenon of declined ability and efficiency of mental and/or physical activities, caused by excessive mental or physical activities, diseases, or syndromes. Acute fatigue is a normal condition that disappears after a period of rest; in contrast, chronic fatigue does not disappear after an ordinary rest. Chronic fatigue impairs daily activities and contributes to various medical conditions and death. In addition, many people complain of chronic fatigue. It would thus be of great value to clarify the mechanisms underlying chronic fatigue and to develop efficient treatment methods to overcome it. Here, we review data primarily from behavioral, neurophysiological, and neuroimaging experiments related to the neural mechanisms underlying chronic fatigue. We propose that repetitive and prolonged overwork and/or stress cause neural damage of a facilitation system, as well as central sensitization and classical conditioning of an inhibition system. We also propose a new treatment strategy for chronic fatigue on the basis of its underlying neural mechanisms.

Drugs acting through 5-hydroxytryptamine (serotonin or 5-HT) systems modulate memory and its alterations, although the mechanisms involved are poorly understood. 5-HT drugs may present promnesic and/or antiamnesic (or even being amnesic) effects. Key questions regarding 5-HT markers include whether receptors directly or indirectly participate and/or contribute to the physiological and pharmacological basis of memory and its pathogenesis; hence, the major aim of this article was to examine recent advances in emergent targets of the 5-HT systems for memory formation and memory alterations. Recent reviews and findings are summarized, mainly in the context of the growing notion of memory deficits in brain disorders (e.g., posttraumatic stress disorder, mild cognitive impairment, consumption of drugs, poststroke cognitive dysfunctions, schizophrenia, Parkinson disease, and infection-induced memory impairments). Mainly, mammalian and (some) human data were the focus. At least agonists and antagonists for 5-HT 1A/1B , 5-HT 2A/2B/2C , 5-HT 3 , 5-HT 4 , 5-HT 6 , and 5-HT 7 receptors as well as serotonin uptake inhibitors seem to have a promnesic and/or antiamnesic effect in different conditions and 5-HT markers seem to be associated to neural changes. Available evidence offers clues about the possibilities, but the exact mechanisms remain unclear. For instance, 5-HT transporter expression seems to be a reliable neural marker related to memory mechanisms and its alterations.

Far transfer between music education and other cognitive skills, such as academic achievement, has been widely examined. However, the results of studies within similar cognitive domains are found to be inconclusive or contradictory. These differences can be traced back to the analytical methods used, differences in the forms of music education studied and differences in neural activation during the processing of these tasks. In order to gain a better picture of the relationships involved, a literature survey was performed in leading databases, such as PubMed/MedLine, psychINFO, ScienceDirect, Embase, ERIC, ASSIA and Jstor from January 2001 to January 2013. All studies included, concerned the far transfer from music education to other cognitive skills in children aged 4–13 years as compared with controls. These studies were independently selected and their quality was assessed by two authors. This systematic review shows the need to address methodological and analytical questions in greater detail. There is a general need to unify methods used in music education research. Furthermore, the hypothesis that intellectual skills, such as mathematics, reading, writing and intelligence can be divided into sub-functions, needs to be examined as one approach to the problems considered here. When this has been done, detailed analysis of cognitive transfer from music education to other disciplines should become possible.