Changes in Visual Cortex in Healthy Aging and Dementia

Brewer, Alyssa A.; Barton, Brian

doi:10.5772/64562

Cited by 8 publications

(14 citation statements)

References 156 publications

(359 reference statements)

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“…The increase in nonspecific errors in the tritan and deutan axes observed in our AD patients suggests that, in addition to the loss of magno- and parvocellular-cells mentioned above, the koniocellular pathway could also be involved due to its association with the blue-yellow spectrum [51]. In addition, it has also been described that patients with AD have a significant reduction in the V4 area, which is a key region that processes colour vision [52,53]. On the other hand, degeneration in the photoreceptor layer has also been described in patients with AD, which is not restricted to a single cone type due to the decrease in melatonin and its antioxidant effects that occur in this pathology [54,55].…”

Section: Discussionmentioning

confidence: 85%

Changes in visual function and retinal structure in the progression of Alzheimer's disease

et al. 2019

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Background Alzheimer’s Disease (AD) can cause degeneration in the retina and optic nerve either directly, as a result of amyloid beta deposits, or secondarily, as a result of the degradation of the visual cortex. These effects raise the possibility that tracking ophthalmologic changes in the retina can be used to assess neurodegeneration in AD. This study aimed to detect retinal changes and associated functional changes in three groups of patients consisting of AD patients with mild disease, AD patients with moderate disease and healthy controls by using non-invasive psychophysical ophthalmological tests and optical coherence tomography (OCT). Methods We included 39 patients with mild AD, 21 patients with moderate AD and 40 age-matched healthy controls. Both patients and controls were ophthalmologically healthy. Visual acuity, contrast sensitivity, colour perception, visual integration, and choroidal thicknesses were measured. In addition, OCT and OCT angiography (OCTA) were applied. Findings Visual acuity, contrast sensitivity, colour perception, and visual integration were significantly lower in AD patients than in healthy controls. Compared to healthy controls, macular thinning in the central region was significant in the mild AD patients, while macular thickening in the central region was found in the moderate AD group. The analysis of macular layers revealed significant thinning of the retinal nerve fibre layer, the ganglion cell layer and the outer plexiform layer in AD patients relative to controls. Conversely, significant thickening was observed in the outer nuclear layer of the patients. However, mild AD was associated with significant thinning of the subfovea and the nasal and inferior sectors of the choroid. Significant superonasal and inferotemporal peripapillary thinning was observed in patients with moderate disease. Conclusions The first changes in the mild AD patients appear in the psychophysical tests and in the central macula with a decrease in the central retinal thickness. When there was a disease progression to moderate AD, psychophysical tests remained stable with respect to the decrease in mild AD, but significant thinning in the peripapillary retina and thickening in the central retina appeared. The presence of AD is best indicated based on contrast sensitivity.

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Section: Discussionmentioning

confidence: 85%

Changes in visual function and retinal structure in the progression of Alzheimer's disease

et al. 2019

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“…Previous studies have shown that neuronal death during normal aging is significantly less as compared to the high cell loss in AD [84]. AD, the most common form of dementia, has been characterized as a progressive neurodegenerative disease that selectively damages neural circuits, and it is distinguished by neurite dystrophy present in about 80% of the aged population having dementia [5,84,103,104]. Age-dependent loss of neurons, decline in synaptic plasticity, and cognitive impairments are often observed in normal aging and neurodegenerative diseases such as AD [84,105,106].…”

Section: Circuit Mechanisms For Normal and Diseased Aging Of Visual Fmentioning

confidence: 99%

“…A great amount of research over the past few decades has shown the dynamic nature of neuroanatomical and functional organization of neural circuits in human, non-human primates, and other species that alter in response to various stimuli [17,39]. Neuroimaging studies have shown lower levels of blood oxygen level dependent (BOLD) activity in V1 of elderly subjects as compared to young adults, while no significant effect on fixation stability was observed in aged adults, which is an important parameter used for visual field map assessments [5,103]. Previous studies discussing various modeling methods of the population receptive field have demonstrated several alterations such as decreased foveal surface area and increased RF sizes in the V1 of elderly subjects as compared to young adults [5,103].…”

Section: Circuit Mechanisms For Normal and Diseased Aging Of Visual Fmentioning

confidence: 99%

“…Neuroimaging studies have shown lower levels of blood oxygen level dependent (BOLD) activity in V1 of elderly subjects as compared to young adults, while no significant effect on fixation stability was observed in aged adults, which is an important parameter used for visual field map assessments [5,103]. Previous studies discussing various modeling methods of the population receptive field have demonstrated several alterations such as decreased foveal surface area and increased RF sizes in the V1 of elderly subjects as compared to young adults [5,103]. These changes may reflect behavioral alterations such as reduced contrast sensitivity and decreased visual acuity and anatomical changes such as reduced thickness of the retinal nerve fiber accompanied by a substantial decline in retinal photoreceptors [5].…”

Section: Circuit Mechanisms For Normal and Diseased Aging Of Visual Fmentioning

confidence: 99%

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Differential Circuit Mechanisms of Young and Aged Visual Cortex in the Mammalian Brain

Mohammed¹

2021

NeuroSci

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The main goal of this review is to summarize and discuss (1) age-dependent structural reorganization of mammalian visual cortical circuits underlying complex visual behavior functions in primary visual cortex (V1) and multiple extrastriate visual areas, and (2) current evidence supporting the notion of compensatory mechanisms in aged visual circuits as well as the use of rehabilitative therapy for the recovery of neural plasticity in normal and diseased aging visual circuit mechanisms in different species. It is well known that aging significantly modulates both the structural and physiological properties of visual cortical neurons in V1 and other visual cortical areas in various species. Compensatory aged neural mechanisms correlate with the complexity of visual functions; however, they do not always result in major circuit alterations resulting in age-dependent decline in performance of a visual task or neurodegenerative disorders. Computational load and neural processing gradually increase with age, and the complexity of compensatory mechanisms correlates with the intricacy of higher form visual perceptions that are more evident in higher-order visual areas. It is particularly interesting to note that the visual perceptual processing of certain visual behavior functions does not change with age. This review aims to comprehensively discuss the effect of normal aging on neuroanatomical alterations that underlie critical visual functions and more importantly to highlight differences between compensatory mechanisms in aged neural circuits and neural processes related to visual disorders. This type of approach will further enhance our understanding of inter-areal and cortico-cortical connectivity of visual circuits in normal aging and identify major circuit alterations that occur in different visual deficits, thus facilitating the design and evaluation of potential rehabilitation therapies as well as the assessment of the extent of their rejuvenation.

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“…Measurements of individual AFMs along the cortical hierarchy will help reveal the distinct stages of top-down and bottom-up auditory processing. In addition, changes in AFMs can be tracked to study how auditory cortex changes under various attentional and working memory tasks and disorders (e.g., [145,[171][172][173][174][175][176][177]).…”

Section: Measuring Attention and Working Memory In Human Afmsmentioning

confidence: 99%

Attention and Working Memory in Human Auditory Cortex

Barton¹,

Brewer²

2020

The Human Auditory System - Basic Features and Updates on Audiological Diagnosis and Therapy

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Human sensory systems are organized into processing hierarchies within cortex, such that incoming sensory information is analyzed and compiled into our vivid sensory experiences. Computations that are common to these sensory systems include the abilities to maintain enhanced focus on particular aspects of incoming sensory information (i.e., attention) and to retain sensory information in a short-term memory store after such sensory information is no longer available (i.e., working memory). In at least the auditory and visual systems, the necessary computational steps to create these experiences take place in cloverleaf clusters of cortical field maps (CFMs). The human auditory CFMs represent the spectral (i.e., tones) and temporal (i.e., period) aspects of sound, which are represented along the cortical surface as two orderly gradients that are physically orthogonal to one another: tonotopy and periodotopy, respectively. Knowledge of the properties of such CFMs is the foundation for understanding the specific sensory computations carried out in particular cortical regions. This chapter reviews current research into auditory nonverbal attention, auditory working memory, and auditory CFMs, and introduces the next steps to measure the effects of attention and working memory across the known auditory CFMs in human cortex using functional MRI. 2Across the cortical hierarchy, there is generally a progressive increase in the complexity of sensory computations from simple sensory stimulus features (e.g., frequency content) to higher levels of cognition (e.g., attention and working memory) [6,13,22]. CFM organization likely serves as a framework for integrating bottom-up inputs from sensory receptors with top-down attentional processing [12,17]. With the recent ability to measure AFMs in the core and belt regions of human auditory cortex along Heschl's gyrus (HG) using high-resolution functional magnetic resonance imaging (fMRI), the stage is now set for investigation into this integration of basic auditory processing with higher-order auditory attention and working memory within human AFMs (Figure 1) [5,12,15,23].This chapter first provides a brief history of research into models of auditory nonverbal attention and working memory, with comparisons to their visual counterparts. Next, we discuss the current state of research into AFMs within human auditory cortex. Finally, we propose directions of future research investigating auditory attention and working memory within these AFMs to illuminate how these higher-order cognitive processes interact with low-level auditory processing. Attention and working memory in human audition Models of attention and working memoryAttention, the ability to select and attend to aspects of the sensory environment while simultaneously ignoring or inhibiting others, is a fundamental aspect of human sensory systems (for reviews, see [24][25][26][27]). Given the limited resources of the human brain, attention allows for greater resources to be allocated to processing of important incoming senso...

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Changes in Visual Cortex in Healthy Aging and Dementia

Cited by 8 publications

References 156 publications

Changes in visual function and retinal structure in the progression of Alzheimer's disease

Changes in visual function and retinal structure in the progression of Alzheimer's disease

Differential Circuit Mechanisms of Young and Aged Visual Cortex in the Mammalian Brain

Attention and Working Memory in Human Auditory Cortex

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