**3. Specific changes occur in early visual cortex during otherwise healthy aging**

In order to carefully evaluate alterations of visual cortex in the age-related neurodegenerative destruction of AD, we must investigate what changes occur across visual cortex during healthy aging [57, 132, 133]. To do so, studies have typically measured healthy visual aging in subjects over the age of 55 with no known age-related diseases or specific, clinically recognized deficits in vision. Major lesions along the retino-cortical visual pathways are not expected to occur in healthy aging, unlike in AD, but subtle retinal and cortical lesions as described below likely contribute to the variations in visual behavior associated with aging.

Lesion studies in young adult human subjects and animal models have outlined general expectations for changes in cortex that underlie the behavioral deficits arising from the loss of or alterations to the retina or visual pathways (**Figure 7**). Consider a retinal lesion that destroys function in the center of vision (i.e., the fovea). In this case, neurons with a pRF entirely within the cortical region to which the lesion projects (i.e., the lesion projection zone, LPZ) will be silenced, causing the cortical activity—and thus the corresponding BOLD signal—to drop to near zero and the distribution of the central eccentricity representation across the surface area of a VFM to shift to be more peripheral, as activity in the foveal representation would be lost (**Figure 7A** and **B**, *top row*). A second set of neurons would have RF centers located within the LPZ, but would have some of the spread of the pRF remain activated by still-healthy retinal regions. Here, the BOLD signal may drop somewhat but not completely, the surface area distribution would still shift toward the periphery, and the pRF centers of these neurons would also be measured as shifting toward the periphery (**Figure 7A** and **B**, *middle row*). Finally, a third set of neurons would have pRF centers outside of the LPZ, but would have some of the spread of the pRF still within the LPZ. Measurements of these neurons would likely show little drop in BOLD signal, a small shift of surface area distributions to the periphery, and also a small shift of pRF centers toward the periphery (**Figure 7A** and **B**, *bottom row*).

Anatomical and neuroimaging measurements from the few studies to date examining VFM changes in healthy aging have demonstrated several such changes in aging visual pathways that may contribute to such age-related behavioral changes as a decline in visual acuity, deficits in contrast sensitivity, and changes in color vision and visual-spatial attention. Next, we examine how such cortical changes may contribute to these healthy-aging behavioral deficits.

**Figure 7. Schematic of the predicted effects of a retinal or cortical lesion on receptive field responses. (A)** Solid black disks and the black-outlined teal circles around them indicate the preferred center and spread of a neuron's receptive field, respectively. Each row represents neurons with preferred centers at one specific eccentricity under normal condi‐ tions. **(B)** The gray-shaded regions indicate the lesion projection zone (LPZ) arising from retinal or cortical neuronal loss. The interaction of the LPZ with a neuron's receptive field is expected to shift the receptive field center more pe‐ ripherally relative to normal conditions, as indicated by the black arrows. *Top:* RFs of these neurons are completely obscured by the LPZ. *Middle:* RFs of these neurons are partially obscured by the LPZ, and the RF centers fall within the LPZ. *Bottom:* RFs of these neurons are partially obscured by the LPZ, and the RF centers fall outside the LPZ. For addi‐ tional discussions, see [8, 9, 12, 16].

#### **3.1. Reductions in cortical activity**

A change in cortical activity, whether from a change in peripheral inputs to a particular region (**Figure 7B**, *top row*) or from general changes in cortical responsivity with aging, is a likely component of such aging deficits as a decrease in effective peripheral vision and problems with color discrimination. Given the increase in our knowledge of the role of certain cortical regions with specific behaviors, it is particularly interesting to examine changes in the level of activity of individual VFMs between healthy young adult and aging subjects.

### *3.1.1. Shrinkage of the useful field of view*

**Figure 7. Schematic of the predicted effects of a retinal or cortical lesion on receptive field responses. (A)** Solid black disks and the black-outlined teal circles around them indicate the preferred center and spread of a neuron's receptive field, respectively. Each row represents neurons with preferred centers at one specific eccentricity under normal condi‐ tions. **(B)** The gray-shaded regions indicate the lesion projection zone (LPZ) arising from retinal or cortical neuronal loss. The interaction of the LPZ with a neuron's receptive field is expected to shift the receptive field center more pe‐ ripherally relative to normal conditions, as indicated by the black arrows. *Top:* RFs of these neurons are completely obscured by the LPZ. *Middle:* RFs of these neurons are partially obscured by the LPZ, and the RF centers fall within the LPZ. *Bottom:* RFs of these neurons are partially obscured by the LPZ, and the RF centers fall outside the LPZ. For addi‐

A change in cortical activity, whether from a change in peripheral inputs to a particular region (**Figure 7B**, *top row*) or from general changes in cortical responsivity with aging, is a likely

tional discussions, see [8, 9, 12, 16].

286 Update on Dementia

**3.1. Reductions in cortical activity**

Decrease in sensitivity across the visual field and a shrinkage of the useful field of view have been measured in behavioral studies of healthy aging subjects, with greater impairments in peripheral vision [28, 29, 38, 134]. The useful field of view is defined as the visual area in which information can be acquired while the eyes are held steady on a single fixation point. Within the useful field of view, a subject is able to detect, identify and discriminate visual stimuli without making an eye movement away from central fixation.

Measurements of visual search, in which the subject seeks a visual target (e.g., a single "T") hidden among distractors (e.g., many "L"s) demonstrated that there is a reduction as a function of increasing age in the size of the visual field used in the visual search task [38]. This reduction in the useful visual field size arises from a decrease in useful peripheral vision, but can be seen in healthy aging subjects without any clinical conditions affecting the optics of the eye. Although relative lens density increases with age and average pupil size is reduced, these changes do not account for the loss of useful peripheral vision or for the decrease in visual field sensitivity, which suggests that age-related visual field sensitivity changes are primarily due to neural losses rather than preretinal issues.

Evidence for how these changes may arise in cortex has been found with fMRI measurements of the BOLD signal modulation (measured as coherence) in early VFMs. In our recent study that used fMRI with pRF modeling to measure healthy aging VFM characteristics, the coher‐ ence of the peripheral 7–10° representation in V1 was found to be significantly lower in aging subjects than in youthful subjects (**Figure 8A**) [36, 37]. No significant differences in more peripheral regions of V2, V3, or hV4 were measured between subject groups (**Figure 8B–D**), so it is possible that the decrease in V1 alone—the primary visual cortex through which the majority of visual inputs pass—is sufficient to drive the behavioral changes. Due to the difficulty in setting up an fMRI paradigm to measure the visual periphery beyond 15–20°, no studies have yet investigated whether additional changes occur in this region across these VFMs.

Similarly, electrophysiology measurements of normally aging macaque monkeys have shown a significant decrease in the response-to-noise ratio and an increase in the neural-response variability in V1 and in the motion-selective medial temporal area (MT, also known as V5) in aging macaque monkeys [43]. These changes in cortical signals have been suggested to possibly arise from a degradation of inhibitory intra-cortical circuits in aging. With such degradations, the selectivity of particular neurons likely decreases, leading to greater activity arising from noise in a particular visual pathway and a consequent decrease in accurate signal-to-noise visual discrimination. In addition, anatomical studies of the visual pathway changes in normal aging humans demonstrate a decline in the retinal-nerve-fiber-layer thickness [46, 54] and a loss of retinal rod photoreceptors [49, 50, 53], both of which could cause a decrease in coherence

**Figure 8. Average measurements of BOLD response in coherence for visual field maps in young, healthy aging, and mild Alzheimer's disease subjects.** Blue lines represent data from healthy young subjects, red lines represent data from healthy aging subjects, and green lines represent data from AD subjects. Each line represents data measured in individual subjects and then averaged by iso-eccentricity band across hemispheres. Regions for each measurement shown to be significant are shown along the *x*-axis with shaded gray regions for comparisons between aging and youthful subjects and solid black lines for comparisons between AD and aging subjects. Dotted black lines represent regions shown to be marginally significant for comparisons between AD and aging subjects. Error bars indicate S.E.M. **(A)** V1; **(B)** V2; **(C)** V3; **(D)** hV4. Note the consistency for the youthful subjects and the somewhat greater variability for the healthy aging subjects. Also note both the decreased coherence and increased measurement variability for the AD subjects. Data were collected from [36, 37, 39].

#### *3.1.2. Problems with color discrimination*

Aging subjects frequently demonstrate losses in color discrimination—the ability to tell color hues apart—especially along the blue-yellow axis. While these issues can be partially attrib‐ uted to changes in the aging lens [35] or to a loss of retinal S-cone (short wavelength) photo‐ receptors, which have a peak selectivity for shorter wave lengths of light [29, 30, 135], growing evidence points to additional concurrent neural changes underlying these deficits (e.g., [27, 37, 136]). For example, after corrections for preretinal losses, the decrease in the sensitivity of

S-cone pathways was found to be approximately 0.09 log units per decade in central vision, and these reductions became larger with measurements across the peripheral visual field to 30° [27]. M-cone (middle wavelength) and L-cone (long wavelength) pathways showed similar but not as severe age-related losses, with a decrease per decade of approximately 0.06–0.70 log units. Only some of this loss can be attributed to retinal changes, with the rest arising in central visual pathways.

in peripheral V1 and subsequent VFMs as well as a reduction in the general visual field

**Figure 8. Average measurements of BOLD response in coherence for visual field maps in young, healthy aging, and mild Alzheimer's disease subjects.** Blue lines represent data from healthy young subjects, red lines represent data from healthy aging subjects, and green lines represent data from AD subjects. Each line represents data measured in individual subjects and then averaged by iso-eccentricity band across hemispheres. Regions for each measurement shown to be significant are shown along the *x*-axis with shaded gray regions for comparisons between aging and youthful subjects and solid black lines for comparisons between AD and aging subjects. Dotted black lines represent regions shown to be marginally significant for comparisons between AD and aging subjects. Error bars indicate S.E.M. **(A)** V1; **(B)** V2; **(C)** V3; **(D)** hV4. Note the consistency for the youthful subjects and the somewhat greater variability for the healthy aging subjects. Also note both the decreased coherence and increased measurement variability for the AD

Aging subjects frequently demonstrate losses in color discrimination—the ability to tell color hues apart—especially along the blue-yellow axis. While these issues can be partially attrib‐ uted to changes in the aging lens [35] or to a loss of retinal S-cone (short wavelength) photo‐ receptors, which have a peak selectivity for shorter wave lengths of light [29, 30, 135], growing evidence points to additional concurrent neural changes underlying these deficits (e.g., [27, 37, 136]). For example, after corrections for preretinal losses, the decrease in the sensitivity of

sensitivity.

288 Update on Dementia

subjects. Data were collected from [36, 37, 39].

*3.1.2. Problems with color discrimination*

Along these lines, fMRI measurements of cortical activity suggest that changes in the cortical color processing pathways may reflect issues with S-cone sensitivity and may further contrib‐ ute to problems with color discrimination in normally aging subjects. Interestingly, our measurements of the BOLD coherence in hV4 demonstrated an increase in cortical activity over the central 1–7° of eccentricity in healthy aging relative to youthful subjects (**Figure 8D**) [37]. This coherence increase was consistent across all hemispheres in all subjects. It is possible that aging changes specific to the ventral visual color and form pathway involving V1, V2, and hV4 culminate in increased hV4 activity. In addition, although the total surface areas of V1–3 spanning the tested fields of view did not significantly change with age, the total surface area of hV4 was significantly smaller in the healthy aging subjects, perhaps due to losses in color pathway inputs (**Figure 9**) [36, 37, 39, 45]. Similar increases in occipital activity in healthy aging subjects in studies of visual working memory have been suggested to be a sign of a form of compensatory cognitive activity [55]; perhaps the increased hV4 activity in healthy aging similarly reflects a cognitive attempt to compensate for the reduced size of hV4 and/or for issues with color processing elsewhere in the visual pathways.

**Figure 9. Total surface area measurements for visual field maps in young, healthy aging, and mild Alzheimer's dis‐ ease subjects.** Blue shading again indicates youthful subjects, red shading indicates normal aging subjects, and green shading indicates AD subjects. Total surface area in mm2 for each visual field map was averaged across the individual subject measurements within in each group. "**\***" marks statistically significant differences (*p* < 0.05). Error bars indicate S.E.M. Data were collected from [36, 37].

#### **3.2. Decreases in the cortical magnification of foveal representations**

Cortical magnification is a common property of sensory systems that may arise from the increased cortical representation of a particular region of sensory space important for behavior. A change in the size of a specific part of a cortical representation between species or subject groups would suggest a related change in the functional properties of that region of cortex and possibly in behavior. For example, if the foveal representation of V1 is significantly reduced in extent for a particular patient group, then it is likely that there is a difference between those patients' central visual processing and that of healthy subjects with normally sized foveal representations (e.g., [8, 10, 12, 36, 37]).

Current measurements of cortical magnification usually consider only one dimension of visual space (e.g., position along eccentricity axis) and disregard the other dimension (e.g., position along polar angle axis) [14]. Thus, the cortical magnification factor as a function of position along the eccentricity axis does not reflect the magnification of representation along an isoeccentricity line (i.e., across polar angles). We have recently altered such measurements to provide a measure that takes this "width" across polar angles into account by determining the surface-area-percent distributions for each VFM [3, 36, 37, 88, 111]. This is a measurement of what percentage of the total surface area of a VFM (spanning the tested field of view) is the surface area of the representation of a 1° band of eccentricity. As in cortical magnification, changes in the surface-area-percent distribution within a VFM can propose likely changes in function; for example, decreases in the foveal surface area may correlate with deficits in central vision (**Figure 7B**).

#### *3.2.1. Decline in visual acuity*

Our static visual acuity determines the smallest detail that we can distinguish in a stationary visual target. Such acuity has been shown to decline after 50 years of age, even in healthy aging subjects with good visual correction through glasses or contact lenses [24, 29, 41, 50, 137]. This loss in visual acuity is exacerbated by low contrast or low luminance in the visual scene [29]. As we rely on our central, foveal vision for our highest acuity, changes in foveal representations would be expected as part of a cortical contribution to this age-related decline in visual acuity.

Our pRF measurements of cortical surface area demonstrated just such a change, measuring a significant decrease in the foveal surface-area-percent distributions of early VFMs V1–hV4 for healthy aging subjects relative to young subjects (**Figure 10**, *red* and *blue lines*, respectively) [36, 37]. A second study by Crossland et al. [39] similarly measured a comparable decrease in the proportion of V1 representing the fovea, by comparing foveal eccentricity activations within polar angle measurements. These aging foveal-representation decreases are consistent with the decline in visual acuity seen normally in aging [24, 29, 41, 50, 137]. These measure‐ ments of foveal changes are unlikely to have arisen from unstable eye position, as Crossland et al. [39] demonstrated that aging has no effect on fixation stability, and models of improper fixation do not predict such results [12, 138]. Such a decrease in the size of the aging foveal representations across multiple early VFMs would be expected to lead to a loss in the resolution of cortical processing of visual information within the fovea, thus diminishing visual acuity.

**Figure 10. Surface area distribution as the percentage of total surface area.** Graphs display average surface-area-per‐ cent-distribution measurements for visual field maps in young (*blue lines*), healthy aging (*red lines*), and AD (*green lines*) subjects. Each line represents data measured in individual subjects and then averaged by iso-eccentricity band across hemispheres. Regions for each measurement shown to be significantly different are shown with shaded gray regions for comparisons between aging and youthful subjects **(A)** V1; **(B)** V2; **(C)** V3; **(D)** hV4. Note the relatively increased foveal distribution in the youthful subjects, and the relatively increased peripheral distribution in AD subjects. Error bars indicate S.E.M. Data were collected from [36, 37].

#### *3.2.2. Deficits in spatial and temporal contrast sensitivity*

**3.2. Decreases in the cortical magnification of foveal representations**

representations (e.g., [8, 10, 12, 36, 37]).

vision (**Figure 7B**).

290 Update on Dementia

*3.2.1. Decline in visual acuity*

Cortical magnification is a common property of sensory systems that may arise from the increased cortical representation of a particular region of sensory space important for behavior. A change in the size of a specific part of a cortical representation between species or subject groups would suggest a related change in the functional properties of that region of cortex and possibly in behavior. For example, if the foveal representation of V1 is significantly reduced in extent for a particular patient group, then it is likely that there is a difference between those patients' central visual processing and that of healthy subjects with normally sized foveal

Current measurements of cortical magnification usually consider only one dimension of visual space (e.g., position along eccentricity axis) and disregard the other dimension (e.g., position along polar angle axis) [14]. Thus, the cortical magnification factor as a function of position along the eccentricity axis does not reflect the magnification of representation along an isoeccentricity line (i.e., across polar angles). We have recently altered such measurements to provide a measure that takes this "width" across polar angles into account by determining the surface-area-percent distributions for each VFM [3, 36, 37, 88, 111]. This is a measurement of what percentage of the total surface area of a VFM (spanning the tested field of view) is the surface area of the representation of a 1° band of eccentricity. As in cortical magnification, changes in the surface-area-percent distribution within a VFM can propose likely changes in function; for example, decreases in the foveal surface area may correlate with deficits in central

Our static visual acuity determines the smallest detail that we can distinguish in a stationary visual target. Such acuity has been shown to decline after 50 years of age, even in healthy aging subjects with good visual correction through glasses or contact lenses [24, 29, 41, 50, 137]. This loss in visual acuity is exacerbated by low contrast or low luminance in the visual scene [29]. As we rely on our central, foveal vision for our highest acuity, changes in foveal representations would be expected as part of a cortical contribution to this age-related decline in visual acuity.

Our pRF measurements of cortical surface area demonstrated just such a change, measuring a significant decrease in the foveal surface-area-percent distributions of early VFMs V1–hV4 for healthy aging subjects relative to young subjects (**Figure 10**, *red* and *blue lines*, respectively) [36, 37]. A second study by Crossland et al. [39] similarly measured a comparable decrease in the proportion of V1 representing the fovea, by comparing foveal eccentricity activations within polar angle measurements. These aging foveal-representation decreases are consistent with the decline in visual acuity seen normally in aging [24, 29, 41, 50, 137]. These measure‐ ments of foveal changes are unlikely to have arisen from unstable eye position, as Crossland et al. [39] demonstrated that aging has no effect on fixation stability, and models of improper fixation do not predict such results [12, 138]. Such a decrease in the size of the aging foveal representations across multiple early VFMs would be expected to lead to a loss in the resolution of cortical processing of visual information within the fovea, thus diminishing visual acuity.

Spatial contrast is the difference in luminance (i.e., brightness) or color that makes an object within a visual scene distinguishable from the rest of the scene. Spatial contrast sensitivity, then, is a measure of a subject's ability to distinguish bright and dark aspects of a scene. This ability is a very important part of visual function, especially in situations of low light or glare (e.g., as in night driving), when the contrast between objects and their background is reduced. Spatial contrast sensitivity is commonly measured by a patient's ability to distinguish light and dark gratings, and age-related declines are most notable for gratings of intermediate and high spatial frequency [139, 140]. This problem cannot be eliminated by optimal lens correction [141, 142] or by elevated luminance [18, 141]. Along these lines, Elliot et al. [19, 33] demon‐ strated that the decrease in spatial contrast sensitivity at medium and high spatial frequencies with increasing age is mostly due to retinal and cortical changes rather than optical changes in the eye. The decreases in the surface-area-percent distributions of the V1–hV4 foveal representations in healthy aging compared with young adult subjects are likely to play a role in these spatial-contrast-sensitivity impairments, in addition to the decline in visual acuity described above (**Figure 10**) [36, 37, 39]. As the cortical territory devoted to central visual processing decreases, fewer neurons will be available to subserve behavioral discrimination of differences in spatial contrast.

The visual system also is sensitive to temporal contrast; temporal contrast sensitivity is a measure of the light-level difference (i.e., contrast modulation) required for an observer to be able discriminate a light source as flickering versus steady. Temporal contrast sensitivity is typically measured using a spatially uniform, randomly flickering stimulus. If the stimulus changes too slowly, an observer cannot detect the change, and if the stimulus changes too quickly, it is seen as a steady rather than flickering image. Similar to the problems with spatial contrast, aging subjects have decreased temporal contrast sensitivity at intermediate and high temporal frequencies [22, 25], as well as problems with motion discrimination [21, 32]. As human V1 and V3 have been implicated in motion processing [118, 143], the decreased foveal surface areas of aging V1 and V3 may similarly play a role in these temporal-contrastsensitivity and motion-discrimination deficits (**Figure 10A** and **C**) [141].

#### *3.2.3. Difficulties with visual-spatial attention*

Visual-spatial attention is our ability to focus on a specific stimulus in our visual environment. When we look at a visual scene, our attention is drawn to a handful of locations that contain critical pieces of information. Normal visual processing relies on accurate and efficient use of visual-spatial attention, calibrated over a lifetime of visual experiences. Deficits in visualspatial attention are associated with many neurological and neuropsychiatric disorders (e.g., hemispatial neglect [144], autism [145], schizophrenia [146]), and subtle problems with attention are thought to contribute to issues in healthy aging such as increased difficulty with driving [147, 148].

Measurements in macaque and human visual areas V1, V2, and V4 have demonstrated neural mechanisms in these VFMs possibly subserving selective visual-spatial attention [125, 149– 151]. In humans, the significantly smaller surface areas of V2 from 1° to 7° and from 0° to 3° in V1 and hV4 in aging subjects likely denote issues in the processing of high acuity central vision in these regions. Such changes could then contribute to these deficits in visual-spatial attention, (**Figure 10A, B,** and **D**). In addition, the shrinkage of the useful field of view in aging described above may arise from issues correctly deploying visual-spatial attention to the periphery [28, 29, 31, 134].

#### **3.3. Increases in the size of population receptive fields (pRFs)**

As seen for cortical magnification, the receptive field sizes of sensory neurons suggest sensitivity to key aspects of sensory space. Smaller receptive fields can produce a higher resolution of sensory processing and suggest improved behavioral discrimination. For VFMs V1–hV4 in healthy subjects, the foveal representations are relatively magnified and also contain the smallest receptive fields [3, 14, 36, 92]. As inputs to visual areas are degraded, as from lesions to the retina or earlier visual pathways, these receptive fields tend to change in size (e.g., [8, 10, 12, 16, 152]). Changes can either be an increase in size, as, for example, normal lateral inhibition—which tends to refine and narrow receptive fields—is lost, or be a decrease in size, as inputs to that receptive field drop out (**Figure 7B**).

#### *3.3.1. Enlargement of foveal pRFs likely contributes to many of the behavioral deficits associated with healthy aging*

The visual system also is sensitive to temporal contrast; temporal contrast sensitivity is a measure of the light-level difference (i.e., contrast modulation) required for an observer to be able discriminate a light source as flickering versus steady. Temporal contrast sensitivity is typically measured using a spatially uniform, randomly flickering stimulus. If the stimulus changes too slowly, an observer cannot detect the change, and if the stimulus changes too quickly, it is seen as a steady rather than flickering image. Similar to the problems with spatial contrast, aging subjects have decreased temporal contrast sensitivity at intermediate and high temporal frequencies [22, 25], as well as problems with motion discrimination [21, 32]. As human V1 and V3 have been implicated in motion processing [118, 143], the decreased foveal surface areas of aging V1 and V3 may similarly play a role in these temporal-contrast-

Visual-spatial attention is our ability to focus on a specific stimulus in our visual environment. When we look at a visual scene, our attention is drawn to a handful of locations that contain critical pieces of information. Normal visual processing relies on accurate and efficient use of visual-spatial attention, calibrated over a lifetime of visual experiences. Deficits in visualspatial attention are associated with many neurological and neuropsychiatric disorders (e.g., hemispatial neglect [144], autism [145], schizophrenia [146]), and subtle problems with attention are thought to contribute to issues in healthy aging such as increased difficulty with

Measurements in macaque and human visual areas V1, V2, and V4 have demonstrated neural mechanisms in these VFMs possibly subserving selective visual-spatial attention [125, 149– 151]. In humans, the significantly smaller surface areas of V2 from 1° to 7° and from 0° to 3° in V1 and hV4 in aging subjects likely denote issues in the processing of high acuity central vision in these regions. Such changes could then contribute to these deficits in visual-spatial attention, (**Figure 10A, B,** and **D**). In addition, the shrinkage of the useful field of view in aging described above may arise from issues correctly deploying visual-spatial attention to the periphery [28,

As seen for cortical magnification, the receptive field sizes of sensory neurons suggest sensitivity to key aspects of sensory space. Smaller receptive fields can produce a higher resolution of sensory processing and suggest improved behavioral discrimination. For VFMs V1–hV4 in healthy subjects, the foveal representations are relatively magnified and also contain the smallest receptive fields [3, 14, 36, 92]. As inputs to visual areas are degraded, as from lesions to the retina or earlier visual pathways, these receptive fields tend to change in size (e.g., [8, 10, 12, 16, 152]). Changes can either be an increase in size, as, for example, normal lateral inhibition—which tends to refine and narrow receptive fields—is lost, or be a decrease

sensitivity and motion-discrimination deficits (**Figure 10A** and **C**) [141].

**3.3. Increases in the size of population receptive fields (pRFs)**

in size, as inputs to that receptive field drop out (**Figure 7B**).

*3.2.3. Difficulties with visual-spatial attention*

driving [147, 148].

292 Update on Dementia

29, 31, 134].

Further cortical changes that may contribute to the decreased visual acuity in normal aging include the differences in pRF sizes measured across the early VFMs of healthy aging subjects (**Figure 11**) [19, 26, 33, 36, 50]. Significant increases in pRF sizes are present in the foveal representations across V1, V2, V3, and hV4 from 0° to at least 3° of eccentricity [36, 37]. The ∼2° foveal pRF size in the V1 of aging subjects is near that of the more peripheral pRF sizes (e.g., 5–7° of eccentricity) in young adults [36, 92]. Similarly, V2, V3, and hV4 of the healthy aging subjects contain foveal pRFs comparable in size to the pRF sizes of the more peripheral regions of these VFMs in healthy young subjects [37]. The increased foveal pRF sizes in these VFMs may reflect the decrease in visual acuity seen in healthy aging subjects. The decreased foveal surface area in the VFMs of aging subjects may drive these increases in pRF sizes as a compensatory mechanism, but we do not yet know whether such changes in pRF sizes arise directly within these VFMs during healthy aging or reflect other variations such as loss of retinal ganglion cells or alterations in feedback from higher-order VFMs.

**Figure 11. Average population receptive field size measurements for visual field maps in young, healthy aging, and mild Alzheimer's disease subjects.** Average pRF radius in degrees of visual angle (dva) across each visual field map is shown for young (*blue lines*), healthy aging (*green lines*), and AD (*red lines*) subjects. Each line again represents data measured in individual subjects and then averaged by iso-eccentricity band across hemispheres. Regions for each measurement shown to be significantly different are shown with shaded gray regions for comparisons between aging and youthful subjects and solid black lines for comparisons between AD and aging subjects. Dotted black lines repre‐ sent regions shown to be marginally significant for comparisons between AD and aging subjects **(A)** V1; **(B)** V2; **(C)** V3; **(D)** hV4. Note the generally increased pRF sizes and variability for measurements in aging and AD subjects relative to the youthful subjects. Data were collected from [36, 37].

In addition, the broadening of pRF sizes in the aging foveae of these four early VFMs is also consistent with the other behavioral deficits discussed in the sections above. Loss of resolution through these increased foveal pRF sizes likely underlies the decrease in spatial contrast sensitivity (**Figure 11**). The increased pRF sizes of aging V1 and V3 may similarly play a role in temporal-contrast-sensitivity and motion-discrimination deficits (**Figure 11A** and **C**). With respect to issues with color discrimination [27, 29, 30, 35], we have measured significant differences in pRF sizes in V2 and hV4 out to 5° and 6°, respectively, as well as foveal changes in V1 from 0° to 3° (**Figure 11A, B,** and **D**). It is possible that these greater regions of expanded pRFs in aging subjects are associated with aging changes specific to a ventral visual color and form pathway involving V1, V2, and hV4. Finally, V2 and hV4 both showed increases in pRF sizes across larger foveal and parafoveal regions (**Figure 11B** and **D**). These larger pRF sizes could reflect deficits in the proper tuning of visual-spatial attention and less ability to attend across the entire visual field.
