Eating Disorders in Frontotemporal Dementia and Alzheimer’s Disease: Evaluation of Brain Perfusion Correlates Using 99mTc-HMPAO SPECT with Brodmann Areas Analysis

Abstract

Background:

Eating disorders (ED) in dementia represent a significant impairment affecting patients’ and caregivers’ lives. In frontotemporal dementia (FTD), ED include overeating, sweet food preference, stereotypical eating, and hyperorality, while in Alzheimer’s disease (AD), anorexia and appetite loss are the most common ED.

Objective:

The aim of our study was to highlight Brodmann areas (BAs) implicated specifically in the appearance of ED in FTD and AD.

Methods:

We studied 141 patients, 75 with FTD and 66 with AD. We used the NeuroGam^TM software on the reconstructed single photon emission computed tomography-SPECT data for the automated comparison of BAs perfusion on the left (L) and right (R) hemisphere with perfusion in corresponding BAs of a normal database.

Results:

The FTD group included 27 men and 48 women, age (mean±SD) 65.8±8.5 years, duration of disease 3.4±3.3 years, Mini-Mental State Examination (MMSE) 17.9±8.6, ED score on Neuropsychiatric Inventory (NPI) 4.7±8.5. ED in FTD were correlated with hypoperfusion in right anterior and dorsolateral prefrontal cortices (BAs 10R, 46R), left orbitofrontal cortex (BA 12L), orbital part of the right inferior frontal gyrus (BA 47R), and left parahippocampal gyrus (BA 36L). The AD group included 21 men and 45 women, age (mean±SD) 70.2±8.0 years, duration of disease 3.3±2.4 years, MMSE 20.2±6, ED-NPI score 2.7±3.9. ED in AD were correlated with hypoperfusion in left inferior temporal cortex (BA 20L).

Conclusion:

SPECT imaging with automated mapping of brain cortex could contribute to the understanding of the neural networks involved in the manifestation of ED in dementia.

Keywords

Alzheimer’s disease Brodmann areas eating disorders frontotemporal dementia perfusion SPECT

INTRODUCTION

Eating disorders (ED) in dementia are included in the Neuropsychiatric Inventory (NPI) scale used for the assessment of severity and frequency of neuropsychiatric symptoms (NPSs) in demented subjects, ind-icating the significance of these disorders for the patients’ function, outcome and management, as well as their effect on caregivers [1]. ED in the NPI comprise changes in appetite and food preference and inappropriate eating behaviors [2].

In frontotemporal dementia (FTD), and especially in the behavioral variant of FTD (bvFTD) [3], ED represent a distinguished and early feature of the disease, with a prevalence ranging between 60%to 80%[4]. The spectrum of ED in bvFTD varies and may include overeating and weight gain, sweet food preference, obsessions for specific foods and hyperorality, char-acterized by oral exploration of inappropriate non-food objects [5]. In semantic dementia (SD), patients may exhibit stereotypical eating and food fads or alterations in food preference early in the course of the disease [3, 4], while in the Klüver-Bucy syndrome, which is observed in advanced stages of FTD with bilateral temporal neurodegeneration, the main ED are hyperphagia and hyperorality [3]. In other forms of FTD, limited research has been carried out with respect to ED. In progressive non fluent aphasia (PNFA), the severity of ED is lower compared with SD or bvFTD [6], while in progressive supranuclear palsy (PSP), binge eating has been described in several cases [7, 8].

In Alzheimer’s disease (AD), although the principal disorder is cognitive impairment, ED are also present, albeit less common compared with FTD, and their prevalence ranges between 11%to 64%, with a pooled prevalence value of 34%[5, 9]. The main form of ED in AD is anorexia and appetite loss [10], while preference for sweet food has been reported to a lesser proportion of AD cases [5, 9] and hyperorality is rarely seen [11]. Several authors found that the distinct performance of AD and FTD patients in the domain of ED on NPI, helped in the differential diagnosis of dementia [12]. It was also suggested that ED in AD correlate with the duration and severity of the disease [13]; however, they may also occur in mild AD [14]. Loss of appetite and weight in AD increases the risk of malnutrition, institutionalization, and mortality [10 , 15], while the corresponding ED in FTD represent a source of various health complications which may potentially become fatal, especially in case of hyperorality [3].

Although ED have been established as an important characteristic of dementia, the underlying neu-robiology has not been examined extensively and remain to be elucidated. Various anatomical and functional neuroimaging techniques, including nuclear medicine methods, have tried to provide information about the brain circuits involved in the pathogenesis of ED in dementia [16 –21]. Nevertheless, the literature remains relatively limited and in several cases with contradictory results, which may reflect the complexity of eating control in human brain and the insult of different brain networks due to neurodegeneration in various forms of dementia.

The aim of this study was to evaluate brain perfusion in correlation with ED in FTD and AD patients using single photon emission computed tomography (SPECT) and Brodmann areas (BAs) analysis, in or-der to highlight BAs related with specific neuroche-mistry impairments implicated in the appearance of ED in these types of dementia. The findings of this study would guide the application of the appropriate therapy or the development of new disease specific treatments. In previous published studies [17, 22], the researchers used the region-of-interest (ROI) app-roach focused on arbitrary selected brain areas which are considered to be implicated in these disorders, precluding other brain regions that would be involved in the pathogenesis of ED. On the contrary, in this study we included the whole brain cortex to investi-gate unexpected brain regions potentially involved in the pathogenesis of ED. Moreover, we compared brain perfusion in our study groups with perfusion of normal subjects of the same age, while other res-earchers performed semi-quantitative evaluation of perfusion using as reference a region of the patient’s own brain. The degree of possible degeneration and the resulting hypoperfusion of the reference area using this technique may have influenced the results in these studies.

MATERIALS AND METHODS

Patients

We studied 141 patients examined between 2010 and 2013 in an outpatient Memory Clinic. We used the Diagnostic and Statistical Manual-IV (DSM-IV) criteria [23] for the clinical diagnosis of dementia. Sixty six patients received the diagnosis of AD according to the National Institute on Aging and the Alzheimer’s Association criteria [24], and 75 patients received the diagnosis of FTD according to the appropriate criteria [25 –27]. All the patients underwent a neuropsychological evaluation with a battery of tests including the Mini-Mental State Examination (MMSE) for dementia rating [28], the Addenbrook’s Cognitive Examination-Revised (ACE-R) [29], and the NPI for the evaluation of ED [1]. NPI was administered to caregivers and information about ED was acquired from them. If they responded positive for the presence of ED, then they were asked all the specific questions on this domain which included loss or increase of appetite, loss or gain of body weight, changes in eating behavior (for example too much food in the patient’s mouth at once), changes in the kind of food the patient liked such as eating too many sweets or other specific kinds of food, development of eating behaviors like eating exactly the same kind of food every day or eating the food in exactly the same order and other changes in appetite or eating that have not been asked about. The caregivers rated the frequency and the severity of the symptom on a 4-point and 3-point scale, respectively, as well as the distress the symptom causes on caregivers on a 5-point scale.

We performed magnetic resonance imaging (MRI) in all patients for the exclusion of vascular or structural brain lesions. Patients in our study had minimal cerebrovascular disease (Fazekas 0,1). Patients with psychiatric or other neurological disorders, according to their clinical history or the information received from their families or caregivers and the neuropsychological tests, as well as pregnant women, were excluded from the study.

All patients or their caregivers gave informed consent prior to the study according to the Hospital Ethics Committee guidelines based on the ethical guidelines of the Helsinki Declaration of 1975, as revised in 2000. Written directions on radioprotection were also given to all patients prior to the study.

SPECT studies

All the patients were injected intravenously 740 MBq of ^99 mTechnetium (^99 mTc) hexamethyl propylene amine oxime (HMPAO-Ceretec, Nycomed Amersham Sorin S.R.L., GE Healthcare Amersham Health). SPECT studies were performed 20–30 min after the administration of radiopharmaceutical, on a dual-head gamma camera (ADAC Forte) equipped with low-energy ultra-high resolution parallel-hole collimators. SPECT was conducted according to the European Association of Nuclear Medicine (EANM) guidelines [30] and acquisition parameters included step-and-shoot mode (128 projections, 35 sec/pro-jection, radius of rotation ∼15 cm, angular sampling < 3°), 128×128 matrix and photopeak centered at 140 keV with a symmetrical 10%window, resulting in acquiring over 5 million counts. Filtered back projection technique was used for reconstruction and smoothing was performed with a Generic Wiener filter.

We used the NeuroGam^TM software (Segami-Co-rporation, http://www.segamicorp.com) and a predefined BAs template for the automated comparison of BAs perfusion on the left (L) and right (R) hemisphere, in each patients’ group with BAs perfusion of a normal subjects database (provided by the software) of the same age, as we have previously described [31]. The software provides anatomical co-registration of brain SPECT data in the Talairach space using standard anatomical points, after the reorientation of the three-dimensional volume of each brain and the correction for lateral deviations. SPECT acquisition parameters in our study were the same used for the age corresponding normal subjects. Perfusion values are expressed as standard deviation (SD) differences.

Statistical analysis

Quantitative variables were expressed as mean (standard deviation). Qualitative variables were exp-ressed as absolute and relative frequencies. Partial correlation coefficients were used to explore the ass-ociation of BAs perfusion, when compared with healthy subjects, with ED in AD and FTD patients after controlling for sex, age, and MMSE. Partial correlation was used as a measure of the strength and direction of relationship between two continuous variables whilst controlling for the effect of other variables. It does not make the distinction between independent and dependent variables but reflects a multiple regression model. All reported p values are two-tailed. Statistical significance was set at p < 0.05 and analyses were conducted using SPSS statistical software (version 22.0).

RESULTS

Sample consisted of 66 AD and 75 FTD patients. Demographic and clinical characteristics for the two groups are presented in Table 1. The FTD group consisted of 28 bvFTD, 29 SD, 12 PNFA, and 6 PSP patients. The AD and FTD groups consisted of 21 men/45 women and 27 men/48 women, respectively. Age, duration of disease, and education (years, mean±sd), in AD patients were 70.2±8.0, 3.3±2.4, and 9.7±4.9, respectively. The corresponding values in FTD were 65.8±8.5, 3.4±3.3, and 10.6±4.8, respectively.

Table 1

Characteristics of AD and FTD groups

	AD	FTD
	N = 66	N = 75
	N (%)	N (%)
Sex
Men	21 (31.8)	27 (36)
Women	45 (68.2)	48 (64)
Age (y), mean (SD)	70.2 (8.0)	65.8 (8.5)
Special medical diagnosis		bvFTD 28 (37.3)
		SD 29 (38.7)
		FTD-PNFA 12 (16)
		FTD-PSP 6 (8)
Duration of disease (y), mean (SD)	3.3 (2.4)	3.4 (3.3)
Years of education, mean (SD)	9.7 (4.9)	10.6 (4.8)
MMSE, mean (SD)	20.2 (6)	17.9 (8.6)
ACE-R, mean (SD)	58 (18.5)	50.5 (25.7)
ED - NPI score, mean (SD)	2.7 (3.9)	4.7 (8.5)

AD, Alzheimer’s disease; FTD, frontotemporal dementia; bvFTD, behavioral variant FTD; SD, semantic dementia; PNFA, progressive non fluent aphasia; PSP, progressive supranuclear palsy; MMSE, Mini-Mental State Examination; ACE-R, Addenbrook’s Cognitive Examination-Revised; ED, eating disorders; NPI, Neuropsychiatric Inventory; mean (SD), mean (standard deviation).

Table 2 shows correlation coefficients of ED in AD group with BAs perfusion, when compared with healthy subjects. ED were significantly and negatively correlated only with left inferior temporal cortex (BA 20L) (Fig. 1).

Table 2

Correlation coefficients of ED with BAs perfusion, when compared with healthy subjects, in AD group

		ED
BA 20L	r	–0.265^*
	P	0.044

^*indicates significant correlations after controlling for sex, age, and MMSE. ED, eating disorders; BAs, Brodmann areas; AD, Alzheimer’s disease; MMSE, Mini-Mental State Examination.

Fig. 1

99mTc-HMPAO SPECT of a patient with Alzheimer’s disease and eating disorders (Neuropsychiatric Inventory score = 12). Comparison with normal subjects of the same age using the NeuroGam^TM software (A). Correlation of eating disorders with hypoperfusion in left inferior temporal cortex - Brodmann area 20L (B).

Correlation coefficients of ED with BAs perfusion, when compared with healthy subjects, in FTD group (Table 3) revealed a significant and negative correlation with right anterior and dorsolateral prefrontal cortices (BAs 10R, 46R), left orbitofrontal cortex (BA 12L), orbital part of the right inferior frontal gyrus (BA 47R) and left parahippocampal gyrus (BA 36L) (Fig. 2).

Table 3

Correlation coefficients of ED with BAs perfusion, when compared with healthy subjects, in FTD group

		ED
BA 10R	r	–0.267^*
	P	0.022
BA 12L	r	–0.277^*
	P	0.028
BA 36L	r	0.275^*
	P	0.019
BA 46R	r	–0.269^*
	P	0.021
BA 47R	r	–0.265^*
	P	0.023

^*indicates significant correlations after controlling for sex, age, and MMSE. ED, eating disorders; BAs, Brodmann areas; FTD, frontotemporal dementia; MMSE, Mini-Mental State Examination

Fig. 2

99mTc-HMPAO SPECT of a patient with Frontotemporal dementia and eating disorders (Neuropsychiatric Inventory score = 8). Comparison with normal subjects of the same age using the NeuroGam^TM software (A). Correlation of eating disorders with hypoperfusion in right anterior and dorsolateral prefrontal cortex, left orbitofrontal cortex, orbital part of the right inferior frontal gyrus, and left parahippocampal gyrus - Brodmann areas 10R, 12L, 36L, 46R, and 47R (B).

DISCUSSION

In this study we investigated the perfusion correlates of ED in FTD and AD patients using SPECT and BAs analysis in order to identify specific BAs associated with altered appetite and eating behaviors in these forms of dementia.

According to the current knowledge, appetite and eating control in normal subjects are mediated by a network of brain areas where the hypothalamus represents a key structure [32, 33]. The network also includes other limbic system structures and their connecting areas (such as nucleus accumbens, limbic thalamus, amygdala, hippocampus, and entorhinal, parahippocampal, prefrontal, orbitofrontal and cingulated cortices, ventral tegmental area, and olfactory bulbs) and the insula, which are implicated in the cognitive aspects and rewarding impacts of food, as well as various neurotransmitter systems [32 –34]. Damage to the hypothalamus results in increase or decrease of appetite, while complex eating abnormalities have also been observed subsequent to lesions in specific areas of frontal and temporal lobes [35].

ED in FTD

It is considered that ED in FTD represent impairment of an integrated network which includes the orbitofrontal and prefrontal cortices, the temporal pole, the amygdala, the insula, and posterior hypothalamus [2 , 36]. Abnormal dietary and eating behaviors in FTD correlate with neurodegeneration affecting specifically the right hemisphere [19 , 38].

We found that ED in FTD patients were correlated with hypoperfusion in right anterior and dorsolateral prefrontal cortices (BAs 10R, 46R), left orbitofrontal cortex (BAs 12L), orbital part of inferior frontal gyrus (posterior lateral) on the right (BA 47R) and left parahippocampal gyrus (BA 36L). Our findings are generally in accordance with the findings of other studies where ED are associated with atrophy and hypoperfusion [19–21 , 37–39] in the above areas. The association of orbitofrontal cortex with specific eating behaviors is rather the most common finding in the majority of studies. The orbitofrontal cortex is considered to play a primary role in the organization of feeding in response to internal and external behavioral cues [40]. The orbitofrontal and prefrontal cortices receive inputs from the primary taste cortex in the insula and the adjacent frontal operculum. The primary taste cortex integrates various features of food to form the flavor perception which leads to food selection [41, 42]. Signals from the primary taste cortex to the prefrontal and orbitofrontal cortices undergo processing for the comparison of new food experiences with old ones and storage new, or update past information related to food. Neuroimaging studies have shown an implication of orbitofrontal cortex in taste processing suggesting the presence of a secondary taste center in this area [43, 44]. Therefore, it is likely that orbitofrontal cortex represents the reward value of taste which decreases when satiety has been achieved [42, 45]. Distinct subregions of orbitofrontal cortex are implicated in different reward values. The medial region is related to the reward value of many different pleasant reinforcers including gustatory and olfactory signals, whereas the posterior lateral region is considered to relate with unpleasant stimuli or nonreward [40 , 45–47]. Prefrontal cortex has been reported to exert a cognitive control on appetite through modulatory actions over the areas implicated in eating [48]. Obese individuals with binge eating disorder demonstrate cognitive deficits in multiple domains related to function of prefrontal cortices [49 –52]. Impairment of prefrontal cortex has been attributed either to direct neurodegeneration or following damage to temporal pole and amygdale which present heavy connection with prefrontal cortex [2 , 36]. In our study we also found a correlation of ED with left parahippocampal gyrus. It has been reported that this area shows alterations in activity related to hunger and satiety [46]. More specifically, it has been found that hunger is associated with increased perfusion to the amygdala [18] and the hippocampal and parahippocampal gyri [53]. Additionally, it is considered to be involved in the pathogenesis of other behavioral disorders such as addiction and compulsion, which may include craving for food and other ED [54, 55].

With respect to specific ED seen in FTD, it is supposed that distinct neural mechanisms are involved in each eating behavior [41]. Neuroimaging studies have tried to highlight the underlying mechanisms of these specific ED in FTD. More specifically, hyperphagia was found to correlate with atrophy in anteromedial orbitofrontal cortices, right ventral ins-ular cortex, striatum and posterior hypothalamus [2 , 56]. It is considered that a right orbitofrontal-insular-striatal circuit integrates internal satiety and environmental food signals and its impairment results in overeating [21, 40]. Pathological sweet food preference was associated with atrophy in posterior lateral orbitofrontal cortices, lateral prefrontal cortex, anterior insula, caudate nucleus and inferior temporal lobe and temporal poles, more intense in the right hemisphere [19, 21], as well as with right insula-striatal reward structures, nucleus accumbens, occipital cortex, and cerebellum [57]. It is hypothesized that dis-ruption of posterolateral orbitofrontal cortices, which integrate gustatory, olfactory and other sensory signals needed for normal taste, from gustatory signals processing center in insula, results in alteration of food preference and persistence for sweets [39 , 58]. High caloric intake was found to correlate with atrophy of cingulate, inferior temporal and occipital cortices, thalamus, hippocampus, cerebellum, lingual gyrus, nucleus accumbens and orbitofrontal cortices, more prominent in the right hemisphere in bvFTD and in the left hemisphere in SD [57]. It seems that in SD, semantic networks have an impact on eating control and ED are the result of loss of semantic knowledge concerning food [59, 60]. Hyperorality in FTD patients is considered to be related with disinhibition which is associated with atrophy in temporal poles [3, 61]. In keeping with this hypothesis, it is suggested that hyperorality may be related to temporal lobe atrophy [3, 62].

Several authors have also reported an association of anterior cingulate cortex with ED in FTD [57, 61]. Anterior cingulate cortex has strong connections with the limbic system, as well as with other regions implicated in appetite such as the orbitofrontal cortex and amygdala [63]. Unlikely, we did not find any correlation of anterior cingulate cortex with ED in our study group of FTD patients. Moreover, other authors found a correlation of atrophy in anterior cingulate cortex with the severity of anorexia nervosa [64], while magnetic resonance spectroscopy studies did not find differences between patients with anorexia or bulimia and controls in the anterior cingulate cortex [65]. Additionally, functional studies have shown activation of anterior cingulate cortex during hunger states or processing of gustatory and olfactory signals [66], suggesting that damage in this region may correlate rather with decreased appetite than with hyperphagia seen in FTD. The conflicting findings of these studies would suggest that anterior cingulate cortex may not be related directly with the specific ED of FTD and could be associated with other NPSs seen frequently in FTD [61]. To our knowledge, no previous imaging studies have been published on ED in patients with PNFA and PSP.

ED in AD

In AD patients, we found a correlation of ED with hypoperfusion in left inferior temporal cortex (BA 20L), an area that has been rarely reported in other studies. Nevertheless, the findings of other authors are also variable. Ismail et al. [17] reported that appetite loss was correlated with hypoperfusion in orbitofrontal cortex and anterior cingulate cortex on the left and relative sparing of the corresponding cortices on the right, as well as of the left middle mesial temporal cortex. However, the authors performed the ROI approach selecting a small number of regions a priori, based on their associations with appetite and weight loss in AD and non-AD patients in previous studies [16 , 68]. However, in the same study, the application of statistical parametric mapping (SPM) and multivariate analysis of variance did not reveal significant differences of perfusion in the above areas between AD patients with or without appetite loss. Other authors have also reported an association of low body mass index (BMI) in dementia with hypometabolism of anterior cingulate cortex [16], while, in contrast with the findings of Ismail et al., a correlation of low BMI with atrophy in mesial temporal cortex has also been described [68]. Taking into account the discordances between the previous described studies, as well as the findings of other studies [65] where anorexic and bulimic subjects did not differ from normals in anterior cingulate cortex, we could hypothesize that this area is not specifically implicated in ED in AD patients.

The possible involvement of temporal lobe (though on the right hemisphere) in ED has been suggested in several case reports where brain lesions in this area have been associated with complex eating behavior disorders [35 , 69–71]. Moreover, evidence from stu-dies in anorexia nervosa patients, suggest the involvement of temporal lobe in this disorder [22 , 72–75]. HMPAO SPECT studies during the acute phase or early-onset of anorexia nervosa showed hypoperfusion of the temporal lobes, especially on the left [22 , 73]. Hypoperfusion in these areas persisted for years, even after feeding and recovery of weight [72 –75]. Atrophy of the left temporoparietal cortex in anorexia nervosa has also been described [76, 77]. In the past, isolated cases of anorexia nervosa have also been described in patients with epileptic foci or structural lesions in temporal lobes suggesting that the underlying cause in anorexia nervosa (and maybe in appetite loss in AD) may be an imbalance in neural networks or circuits, which results in an impaired visuospatial function and visual memory [72 , 78]. Additionally, the direct deposition of amyloid plaques and neurofilament tangles in many hypothalamic nuclei in AD patients has also been considered a possible cause for ED, although the signaling pathways involved have not been clearly understood [79, 80]. It has been reported that lesions in the inferior temporal visual cortex (part of the inferior temporal lobe) produce visual aspects of eating impairments such as a tendency to select non-food [81]. The inferior temporal visual cortex projects to the hypothalamus through its connections with other memory associated areas of the brain such as the hippocampus, the amygdala and the prefrontal cortex, thus forming a way for visual information to reach the hypothalamus [82]. Moreover, recent studies report that each single neuron in inferior temporal visual cortex presents specific response to a specific stimulus and may be linked to unique and specific memories [82, 83]. Neurodegeneration of inferior temporal lobe in AD could disrupt this network and the connection with the lateral hypothalamus which is implicated in the analysis of visual stimuli and learning required for food selection.

It has also been hypothesized that weight loss in AD could be related with defects in the integration or processing of olfactory sensations. Using functional magnetic resonance imaging (fMRI), Suzuki et al. [67] found that decreased activation of the left inferior temporal gyrus in elderly volunteers correlated with impairment of olfactory processing. Growdon et al. found that in cognitive normal elderly subjects, worse olfaction was associated with markers of neurodegeneration compatible with those seen in AD, such as increased amyloid deposition, atrophy of entorhinal cortex, reduced hippocampal volumes and worse episodic memory [84].

With respect to lateralization of the findings, we found hypoperfusion on the left, although in several studies the findings were generally more prominent on the right or bilaterally [16 , 68]. Nevertheless, location in the left temporal lobe has also been described [17], while in a relative recent review assessing the association between NPSs in AD and neuroimaging, it was found that ED were correlated with changes mainly in the left hemisphere [85].

Potential limitations

Our study has several potential limitations. First of all, we did not include cerebrovascular disease as a confounding variable in the analyses. However, our patients had minimal vascular lesions (Fazekas 0,1), while the comparison of their brain perfusion was made with a database of cognitively normal subjects of the same age which are expected to have cer-ebrovascular lesions corresponding to their age. Another potential limitation is the use of filtered backprojection method for reconstruction instead of newer techniques based on iterative algorithms, such as the Ordered Subset–Expectation Maximization (OSEM) [30]. However, EANM guidelines suggest both methods for reconstruction [30]. OSEM method offers several advantages like producing higher visual quality images compared with Filtered backprojection method and correcting various physical events such as attenuation and scatter. However, OSEM produces pixels with very high counts, more prominent at the borders of the image requiring scaling of the final reconstructed data, the contrast of which depends on the true contrast and the object size. On the other hand, filtered backprojection is a linear algorithm, much faster than OSEM and is recommended by various scientific associations including, besides EANM, the National Electrical Manufacturers Association (NEMA), remaining widely used in clinical practice [86]. Finally, the consideration of specific eating disorders in AD and FTD patients was beyond the scope of this study. Moreover, such details were not obtained in all patients due to inability of caregivers to answer appropriately to the specific questions on this domain. However, the existing data showed that AD patients had mainly loss of appetite (77.8%) and loss of weight (38.9%), while FTD patients had mostly increase of appetite (48.5%), change in eating behavior (42.4%) and gain of weight (39.4%).

CONCLUSION

Eating alterations in demented patients may cause serious clinical implications with a harmful impact on health. Neuroimaging techniques provide important information of brain function and the resulting specific ED in dementia. More specifically, brain perfusion SPECT imaging using automated cortex mapping analysis could contribute significantly in the understanding of underlying mechanisms of ED in demented individuals by identifying the specific BAs and their neural networks involved in reward, aversive and satiety. The provided information could be used for the development of new treatments and the application of disease specific modifying therapeutic interventions.

DISCLOSURE STATEMENT

Authors’ disclosures available online (https://www.j-alz.com/manuscript-disclosures/20-1434r1).

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