Our understanding of the organization of the frontal cortex can be traced back to the experimental studies in the late 1800s by Fritsch and Hitzig on the frontal cortex of dogs and the frontal cortex ...of monkeys by Ferrier. These studies and many other studies that followed focused on motor functions, but halfway through the 20th century, very little was understood about the role of the frontal lobe in the control of other functions, and it was generally thought that the frontal lobe did not play a significant role in cognition. One result was that studies of cortical functions in cognition were carried out largely on parietal and temporal cortical regions with surprisingly little interest in the frontal lobe. The first systematic studies of the effects of prefrontal lesions on non-human primates began around 1950, especially by Rosvold and Mishkin in the Laboratory of Psychology at the National Institute of Mental Health (NIMH) in the United States. With her background in development, Pat Goldman joined this laboratory in 1965 and began an examination of the effects of prefrontal lobectomy on behavior in infant rhesus monkeys, both during development and later as the animals grew into adulthood. Her developmental studies were groundbreaking as they demonstrated that the effects of early prefrontal lesions varied with precise age (including prenatal), precise lesion location, behaviors measured, and age at assessment. She also began in parallel extensive studies of the role of the prefrontal cortex for a range of functions (especially working memory) in adult monkeys, which led to an examination of factors that influenced functional outcomes after injury or disease. This research was critical in helping to identify the significant role of the prefrontal cortex in cognition in both normal brains and neurological diseases such as schizophrenia. Her pioneering study demonstrating the role of the prefrontal cortex in cognition led to a remarkable increase in the number of researchers studying prefrontal functions in both non-human primates and rodents. This review will chronicle the key findings in her 35
years studying the prefrontal cortex and illustrate the course she set for generations to follow.
Although the behavioral effects of damage to the frontal lobes date back to at least the late 19th century even midway through the 20th century very little was known about human frontal lobe function ...and there was a general consensus that the frontal lobe did not play a key role in cognition. This all changed when Brenda Milner published a chapter in a 1964 volume entitled:
. Milner's chapter, "Some effects of frontal lobectomy in man," was the first systematic study of the effect of frontal lobe excisions on cognition in human patients. Milner had access to a unique population of frontal excision patients at the Montreal Neurological Institute that were being treated by Wilder Penfield and his associates for a wide range of neurological disorders, including intractable epilepsy. Milner and her colleagues engaged in a more than 50-year study that has had a formidable impact on our understanding of frontal lobe function. Paralleling studies of frontal lobe function in non-humans they influence on understanding the evolution and function of the prefrontal cortex of mammals. Thus, although Brenda Milner is best known for her studies of human memory, she has had an equally important contribution to our understanding of the frontal lobes.
•Aging is associated with a global increase of low-frequency rsEEG power and reduced and slowing of alpha activity.•The enhancement of slow and the reduction of fast oscillations is the most common ...finding in AD.•Graph analysis implicates less efficient interaction between brain regions and supports the disconnection hypothesis of AD.•rsEEG features can be reliable predictors of aMCI at risk for conversion to AD.•Studies show the application of gamma-band stimulation in ameliorating AD.
Aging is associated with alterations in cognitive processing and brain neurophysiology. Whereas the primary symptom of amnestic mild cognitive impairment (aMCI) is memory problems greater than normal for age and education, patients with Alzheimer’s disease (AD) show impairments in other cognitive domains in addition to memory dysfunction. Resting-state electroencephalography (rsEEG) studies in physiological aging indicate a global increase in low-frequency oscillations’ power and the reduction and slowing of alpha activity. The enhancement of slow and the reduction of fast oscillations, and the disruption of brain functional connectivity, however, are characterized as major rsEEG changes in AD. Recent rodent studies also support human evidence of age- and AD-related changes in resting-state brain oscillations, and the neuroprotective effect of brain stimulation techniques through gamma-band stimulations. Cumulatively, current evidence moves toward optimizing rsEEG features as reliable predictors of people with aMCI at risk for conversion to AD and mapping neural alterations subsequent to brain stimulation therapies. The present paper reviews the latest evidence of changes in rsEEG oscillations in physiological aging, aMCI, and AD, as well as findings of various brain stimulation therapies from both human and non-human studies.
Extensive studies indicate that severe acute respiratory syndrome coronavirus (SARS-CoV-2) involves human sensory systems. A lack of discussion, however, exists given the auditory-vestibular system ...involvement in CoV disease 2019 (COVID-19). The present systematic review and meta-analysis were performed to determine the event rate (ER) of hearing loss, tinnitus, and dizziness caused by SARS-CoV-2.
Databases (PubMed, ScienceDirect, Wiley) and World Health Organization updates were searched using combined keywords: 'COVID-19,' 'SARS-CoV-2,' 'pandemic,' 'auditory dysfunction,' 'hearing loss,' 'tinnitus,' 'vestibular dysfunction,' 'dizziness,' 'vertigo,' and 'otologic symptoms.'
Twelve papers met the eligibility criteria and were included in the study. These papers were single group prospective, cross-sectional, or retrospective studies on otolaryngologic, neurologic, or general clinical symptoms of COVID-19 and had used subjective assessments for data collection (case histories/medical records). The results of the meta-analysis demonstrate that the ER of hearing loss (3.1%, CIs: 0.01-0.09), tinnitus (4.5%, CIs: 0.012-0.153), and dizziness (12.2%, CIs: 0.070-0.204) is statistically significant in patients with COVID-19 (Z ≤ -4.469, p ≤ 0.001).
COVID-19 can cause hearing loss, tinnitus, and dizziness. These findings, however, should be interpreted with caution given insufficient evidence and heterogeneity among studies. Well-designed studies and follow-up assessments on otologic symptoms of SARS-CoV-2 using standard objective tests are recommended.
Age-related hearing loss (ARHL) or presbycusis, as the third leading cause of chronic disability in older adults, has been shown to be associated with predisposing cognitive impairment and dementia. ...Tinnitus is also a chronic auditory disorder demonstrating a growth rate with increasing age. Recent evidence stands for the link between bothersome tinnitus and impairments in various aspects of cognitive function. Both ARHL and age-related tinnitus affect mental health and contribute to developing anxiety, stress, and depression. The present review is a comprehensive multidisciplinary study on diverse interactions among ARHL, tinnitus, and cognitive decline in older adults. This review incorporates the latest evidence in prevalence and risk factors of ARHL and tinnitus, the neural substrates of tinnitus-related cognitive impairments, hypothesized mechanisms concerning the association between ARHL and increased risk of dementia, hearing amplification outcomes in cases with ARHL and cognitive decline, and preliminary findings on the link between ARHL and cognitive impairment in animal studies. Given extensive evidence that demonstrates advantages of using auditory amplification in the alleviation of hearing handicap, depression, and tinnitus, and the improvement of cognition, social communication, and quality of life, regular hearing screening programs for identification and management of midlife hearing loss and tinnitus is strongly recommended.
•Chronic noise exposure dysregulates the neuroendocrine system leading to hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis.•Stress hormones adversely affect cell biology and neuronal ...circuitry leading to impairment in behavior.•Enduring dysregulation of the HPA-axis is the most mechanism associated with the harmful noise effects.•Noise stress shows a causative association with diverse landmarks of Alzheimer’s disease (AD) with a hyper-susceptibility in females.•Functional and Neuroimaging studies are suggested to quantify the contribution of noise in predisposing AD in human.
This review examines the adverse impacts of different noise exposure paradigms on the neuroendocrine system, hippocampal and neocortical structures, cognitive performances, and the development of Alzheimer's disease (AD)-like neuropathological changes in the brain of laboratory animals. Studies were reviewed in three periods during the lifespan including: adult animals exposed to noise, female rodents exposed to noise during gestation, and offspring exposed to noise during the prenatal period. Findings imply that chronic noise exposure dysregulates the neuroendocrine system leading to hyperactivation of the sympathetic divisions of the autonomic nervous system (i.e., the hypothalamic-pituitary-adrenal (HPA)-axis), and increases stress hormones that affect brain and behaviour. Enduring dysregulation of the HPA-axis was the most discussed mechanism for the harmful effect of noise during the lifespan. Studies also suggest a causative association of noise with diverse indicators of the AD-like neuropathology in rodents and a hypersusceptibility in females. The results indicate the importance of future neuroimaging studies to quantify the potential contribution of noise in predisposing cognitive decline and preclinical signs of dementia in humans.
Although traffic noise exposure is a well-known environmental pollutant whose negative health effect has been discussed in different aspects of the human life, only a few animal studies have tackled ...this issue as a cohort study, which is not feasible to be addressed in human studies. In addition to the deleterious impact of the daytime noise on well-being, chronic nocturnal noise can also disturb sleep and affects physical and mental health, but to date, little research has examined the neurobiological effects of light/dark cycles of traffic noise exposure. We investigated the effects of light/dark cycles and sex on the impact of chronic traffic noise exposure on mouse brain structure-function. The mice were randomly assigned to either one of two stress conditions or a control condition. Animals were exposed to traffic noise on either the light-cycle (LC) or dark-cycle (DC) for 30 days. Traffic noise exposure caused the hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, anxiety-like behavior, impairments in learning and memory, dysfunction in balance and motor coordination, and a reduction in variety of brain measures including a brain volume, medial prefrontal cortex (mPFC) area, cortical thickness, hippocampal volume, amygdala area, and the neural density in mPFC and dentate gyrus. All behavioral and brain measures revealed adverse effects of the chronic noise stress irrespective of the LC/DC exposure or sex. Our findings were a re-emphasis on the significance of noise prevention and mitigation strategies for public health.
•Chronic traffic noise stress markedly entailed the HPA axis hyperactivity.•It caused anxiety-like behavior and impairments in memory and motor coordination.•It significantly reduced neural density and brain volume in some cortical and limbic structures.•Nocturnal exposure impaired brain and behavior as large as the daytime stress.•Findings re-emphasis the significance of noise prevention and mitigation strategies for public health.
Extensive evidence supports the association between age‐related hearing loss (ARHL) and cognitive decline. It is, however, unknown whether a causal relationship exists between these two, or whether ...they both result from shared mechanisms. This paper intends to study this relationship through a comprehensive review of MRI findings as well as evidence of cellular alterations. Our review of structural MRI studies demonstrates that ARHL is independently linked to accelerated atrophy of total and regional brain volumes and reduced white matter integrity. Resting‐state and task‐based fMRI studies on ARHL also show changes in spontaneous neural activity and brain functional connectivity; and alterations in brain areas supporting auditory, language, cognitive, and affective processing independent of age, respectively. Although MRI findings support a causal relationship between ARHL and cognitive decline, the contribution of potential shared mechanisms should also be considered. In this regard, the review of cellular evidence indicates their role as possible common mechanisms underlying both age‐related changes in hearing and cognition. Considering existing evidence, no single hypothesis can explain the link between ARHL and cognitive decline, and the contribution of both causal (i.e., the sensory hypothesis) and shared (i.e., the common cause hypothesis) mechanisms is expected.
Extensive evidence supports the association between age‐related hearing loss and cognitive decline. It is, however, unknown whether a causal relationship exists between these two, or whether they both result from shared mechanisms. This paper intends to study this relationship through a comprehensive review of MRI findings as well as evidence of cellular alterations.
Critical period regulation across multiple timescales Reh, Rebecca K.; Dias, Brian G.; Nelson, Charles A. ...
Proceedings of the National Academy of Sciences - PNAS,
09/2020, Letnik:
117, Številka:
38
Journal Article
Recenzirano
Odprti dostop
Brain plasticity is dynamically regulated across the life span, peaking during windows of early life. Typically assessed in the physiological range of milliseconds (real time), these trajectories are ...also influenced on the longer timescales of developmental time (nurture) and evolutionary time (nature), which shape neural architectures that support plasticity. Properly sequenced critical periods of circuit refinement build up complex cognitive functions, such as language, from more primary modalities. Here, we consider recent progress in the biological basis of critical periods as a unifying rubric for understanding plasticity across multiple timescales. Notably, the maturation of parvalbumin-positive (PV) inhibitory neurons is pivotal. These fast-spiking cells generate gamma oscillations associated with critical period plasticity, are sensitive to circadian gene manipulation, emerge at different rates across brain regions, acquire perineuronal nets with age, and may be influenced by epigenetic factors over generations. These features provide further novel insight into the impact of early adversity and neurodevelopmental risk factors for mental disorders.
Auditory deprivation following congenital/pre‐lingual deafness (C/PD) can drastically affect brain development and its functional organisation. This systematic review intends to extend current ...knowledge of the impact of C/PD and deafness duration on brain resting‐state networks (RSNs), review changes in RSNs and spoken language outcomes post‐cochlear implant (CI) and draw conclusions for future research. The systematic literature search followed the PRISMA guideline. Two independent reviewers searched four electronic databases using combined keywords: ‘auditory deprivation’, ‘congenital/prelingual deafness’, ‘resting‐state functional connectivity’ (RSFC), ‘resting‐state fMRI’ and ‘cochlear implant’. Seventeen studies (16 cross‐sectional and one longitudinal) met the inclusion criteria. Using the Crowe Critical Appraisal Tool, the publications' quality was rated between 65.0% and 92.5% (mean: 84.10%), ≥80% in 13 out of 17 studies. A few studies were deficient in sampling and/or ethical considerations. According to the findings, early auditory deprivation results in enhanced RSFC between the auditory network and brain networks involved in non‐verbal communication, and high levels of spontaneous neural activity in the auditory cortex before CI are evidence of occupied auditory cortical areas with other sensory modalities (cross‐modal plasticity) and sub‐optimal CI outcomes. Overall, current evidence supports the idea that moreover intramodal and cross‐modal plasticity, the entire brain adaptation following auditory deprivation contributes to spoken language development and compensatory behaviours.
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