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1 Behaviour in FTD-ALS was dominated by apathy.
2 of which were dystonia, speech disorder, and apathy.
3 behavioural dysfunction with high levels of apathy.
4 thway in cognitively intact PD patients with apathy.
5 diminished sustained attention, fatigue, and apathy.
6 sion was only 2.62% compared with 14.60% for apathy.
7 observed here might be a useful correlate of apathy.
8 enia patients with high versus low levels of apathy.
9 isorders showing frontal lobe involvement in apathy.
10 ported the role of the anterior cingulate in apathy.
11 nsions of affective flattening and avolition-apathy.
12 cipants (176 cognitively normal), 52 had MBI-apathy.
13 E=0.10, p=0.013) was associated with greater apathy.
14 manifest symptoms of depression, anxiety and apathy.
15 to costs would underpin Huntington's disease apathy.
16 ntribute to motivational deficits, including apathy.
17 activities of daily living-predict emotional apathy.
18 ere included; 20 participants (50%) also had apathy.
19 reduction on Y-BOCS) reporting increases in apathy.
20 1) were additionally associated with greater apathy.
21 posterior cortical areas could contribute to apathy.
22 e closely associated with the development of apathy.
23 .004) and were unchanged in patients without apathy.
24 mited understanding of mechanisms underlying apathy.
25 ased initiation apathy and reduced emotional apathy.
26 e on medication, and assessed in relation to apathy.
27 inically significant) with depression (20%), apathy (15%), and irritability (15%) being most common.
28 1.6%]), slowness (23 [71.9%] vs 95 [26.2%]), apathy (23 [71.9%] vs 189 [52.1%]), and motor deteriorat
29 ial symptoms among symptomatic patients were apathy (23%), disinhibition (18%), memory impairments (1
31 ementia, the most frequent disturbances were apathy (36%), depression (32%), and agitation/aggression
32 Depression (56% versus 17%, P = 0.0003), apathy (40% versus 4%, P < 0.0001), disinhibition (16% v
34 parkinsonism (95.2% of patients), depression/apathy (71.4%), respiratory symptoms (66.7%) and weight
35 as part of mild behavioural impairment (MBI-apathy), a syndrome defined by emergent and persistent N
36 Huntington's disease is also associated with apathy, a loss of motivation and failure to engage in go
38 showed a greater mean reduction in avolition-apathy (adjusted mean [SE], 1.66 [0.31] vs 2.81 [0.34],
39 ical assessments evaluated depression (GDS), apathy (AES), cognitive status (MMST), mobility (TUG), h
42 e aimed to determine the association between apathy and AD biomarkers when it occurred as part of the
43 nson's Progression Markers Initiative cohort.Apathy and anhedonia were measured using a composite sco
44 ate psychiatric symptoms such as depression, apathy and anxiety are risk factors for or prodromal sym
45 pathology may drive the development of both apathy and anxiety in very early stages of AD, largely i
47 functioning and psychiatric symptoms (e.g., apathy and avolition), but not psychotic symptoms (e.g.,
48 ng correlation was found between measures of apathy and both attenuated P3 amplitude and viewing dura
49 etween latent cognitive processes altered in apathy and brain structure and connectivity in a priori
53 studied in order to interpret the degree of apathy and depression found within the small vessel dise
54 symptoms, e.g. gait and balance impairment, apathy and depression in Alzheimer's disease patients su
55 ession and cognitive impairment; and (ii) if apathy and depression make independent contributions to
58 n of behavioral profiles, differentiation of apathy and depression, characterization of risk factors
59 regions of white matter were associated with apathy and depression, controlling for age, gender and c
60 sel disease is associated with high rates of apathy and depression, thought to be caused by a disrupt
64 ocampal sclerosis, the findings of increased apathy and disinhibition merit further investigation.
65 ia (FTD) is a disease of high heterogeneity, apathy and disinhibition present in all subtypes of FTD
66 sdiagnostic studies, measuring subdomains of apathy and disinhibition, and examining different units
67 egative symptoms (such as social withdrawal, apathy and emotional blunting) and other psychopathologi
69 The ability to measure the components of apathy and impulsivity and their associated neural corre
74 o determine the neurocognitive components of apathy and impulsivity in frontotemporal lobar degenerat
80 obar degeneration provides new insights into apathy and impulsivity, and the need for a joint therape
83 for subgroups (r = 0.49, p = 0.04), whereas apathy and left anterior cingulate NFTs showed a signifi
86 onsignificant trend toward less worsening in apathy and no significant between-group differences in a
88 Elucidating brain networks associated with apathy and poor treatment outcomes can inform interventi
89 nsitivity may be a contributory mechanism to apathy and provide potential new clinical measures for i
93 nxiety or depression, cognitive decline, and apathy), and additional features (fatigue, insomnia, ano
99 demonstrated increased rates of depression, apathy, and other behavioural symptoms in the mildly sym
101 horizontal and vertical saccades, dysphagia, apathy, and progressive cognitive decline, which led to
104 sease course), mood (especially, depression, apathy, and suicidality), personality and behavior (espe
106 ences, even in superficially related traits (apathy-anhedonia and anxiety-compulsive checking) reliab
108 triatal DAT specific binding ratio (SBR) and apathy/anhedonia symptoms, which emerged as PD progresse
110 enetic liability to cognitive impairment and apathy appears to be distinct from other psychiatric sym
111 ral symptoms of sickness such as fatigue and apathy are debilitating and can prevent recuperation.
112 Factor analyses showed that empathy and apathy are distinct constructs, but that affective empat
116 t is, 'negativity bias' (negative valence), 'apathy' (arousal) and 'emotional dysregulation' (cogniti
118 ith anosognosia demonstrated faster onset of apathy as compared to patients without anosognosia.
123 also improved on self-reported and caregiver apathy assessments (P = 0.03 and P = 0.02, respectively)
124 er evidence of effort hypersensitivity, with apathy associated with a faster drift rate towards rejec
125 that the interindividual variability of mood/apathy, attention/memory, and sleep outcomes after subth
126 ual framework for understanding pathological apathy based on this current understanding of normal mot
127 gene variant carriers (>50% patients), with apathy being one of the most common and severe symptoms
128 ine was associated with increasing levels of apathy (beta = -0.284, p = .005) and anxiety (beta = -0.
129 d delay sensitivity was also associated with apathy, both when analysing raw choice and drift rate, w
132 t both drugs improved cognitive function and apathy, but had a stronger effect when used in combinati
135 arkinson's disease, which was more marked in apathy, but not predictive of their individual apathy se
136 dication might be an effective treatment for apathy by increasing reward sensitivity, independent of
140 as significantly reduced in PD patients with apathy compared with nonapathetic patients and healthy c
141 d behavioural changes such as disinhibition, apathy, compulsiveness and loss of empathy were the most
142 interest in the neuropsychiatric syndrome of apathy, conceptualised as a loss of motivation manifesti
144 In contrast, Parkinson's patients without apathy demonstrated significantly increased activation a
145 inally, we relate these findings to clinical apathy, demonstrating the homologies between this basic
146 ips between median fractional anisotropy and apathy, depression and cognitive impairment; and (ii) if
148 gnosis of change across 10 BPSDs (agitation, apathy, depression, delusions, disinhibition, auditory h
149 and completed cognitive testing, measures of apathy, depression, quality of life and diffusion tensor
150 urs examined, 4 correlated with tissue loss: apathy, disinhibition, eating disorders and aberrant mot
151 ignificant correlation was found between the apathy/disinhibition scores and functional connectivity
152 studies, we revise a neurocircuitry model of apathy divided along three subcomponents (cognition/plan
153 as moderate evidence of Huntington's disease apathy drifting faster towards the immediately available
154 activation persistence negatively related to apathy, especially anhedonia, and to anhedonia at T3.
155 asked to complete the DAS, the standardised Apathy Evaluation Scale, and the Geriatric Depression Sc
160 lling of the patient's choices confirmed the apathy group made decisions that were indifferent to the
163 with participants without apathy, those with apathy had lower structural connectivity in the splenium
166 ation (hazard ratio=3.06, 95% CI=1.89-4.93), apathy (hazard ratio=2.26, 95% CI=1.49-3.41), anxiety (h
167 ients with anosognosia had a faster onset of apathy (HR: 2.78, 95% CI: 1.37-5.62, p = 0.01) compared
168 e components, interpreted as reflecting: (i) apathy; (ii) challenging behaviours; and (iii) activitie
170 ral symptom by examining the substructure of apathy in ALS and to determine the reliability and valid
175 del free analysis of choice data showed that apathy in both groups was associated with reduced incent
177 We reviewed all neuroimaging studies of apathy in frontotemporal dementia (FTD) attempting to re
179 low the progression of cognitive decline and apathy in neurological conditions where sleep is disorde
180 uilding upon this work, we hypothesized that apathy in Parkinson's disease should be associated with
186 features were depression and anxiety in CBS, apathy in PSP, with sleep disturbances common in PD.
188 r degeneration was associated with increased apathy, increased disinhibition, and decreased psychosis
190 er, Mini-Mental State Examination score, and apathy/indifference, did not affect the rate of function
191 ally discriminating features (disinhibition, apathy/inertia, loss of sympathy/empathy, perseverative/
205 Here we investigated the hypothesis that apathy is associated with disrupted decision making in e
212 tivation, whilst a cross-cutting approach to apathy is still informative from a framework perspective
214 ients with low apathy levels (N=18) and high apathy levels (N=20) and 12 healthy comparison subjects
215 the impact of surgery and lesion location on apathy levels is clearly warranted using objective, quan
216 avoid pathogens, here we describe a peculiar apathy-like behavior towards PA14 in animals with consti
217 ically induced increased effort-sensitivity, apathy-like symptoms through a cytokine-sensing brainste
218 ehavioral symptoms, including disinhibition, apathy, loss of empathy, perseverative behavior, and hyp
219 bitofrontal cortex in AD, whereas increasing apathy may relate to greater NFT burden in the anterior
220 re stratified by NPS status (MBI-apathy, non-apathy MBI, non-MBI NPS and no-NPS) based on the Neurops
221 res for improved diagnosis and monitoring of apathy.media-1vid110.1093/brain/aww188_video_abstractaww
222 nistered self-report measures of empathy and apathy-motivation to a large sample of healthy people (n
223 Delusion, hallucination, agitation, anxiety, apathy, motor-disturbances, night-time behavior and eati
224 nitiative were stratified by NPS status (MBI-apathy, non-apathy MBI, non-MBI NPS and no-NPS) based on
225 ese processes is likely to contribute to the apathy observed in patients after injury to the frontal
228 mpal sclerosis was associated with increased apathy (odds ratio, 2.60; 95% CI; 1.86-3.66, false disco
230 ential impact of syndromes such as mania and apathy on rehabilitation efforts or pathological crying
231 s, patients showed a significant increase in apathy on the Initiation subscale, and were significantl
233 area including (i) the assessment of either apathy or impulsivity alone, despite their frequent co-e
234 were found to exhibit a higher frequency of apathy (OR, 1.89; 95% CI, 1.09-3.78; P = .03), nighttime
235 nguishing features between the 2 groups were apathy (OR, 4.53; 95% confidence interval [CI], 3.11-6.6
238 es were significantly lower in patients with apathy (P = 0.004) and were unchanged in patients withou
242 al equation modelling results indicated both apathy (r = -0.23, P </= 0.001) and depression (r = -0.4
243 anisotropy was significantly associated with apathy (r = -0.38, P </= 0.001), but not depression (r =
245 (SD) 4.3 (3.2) vs 2.1 (2.1); p=0.001), Lille Apathy Rating Scale (mean (SD) -23.3 (9.6) vs -27.0 (4.7
246 imulation measured by the Person-Environment Apathy Rating-Environment subscale (stimulation clarity,
251 s found from baseline to 6 months in the NPI apathy score in those receiving methylphenidate compared
252 ed in an improved Neuropsychiatric Inventory apathy score, with an estimated -1.32 points (95% CI -2.
255 ctivity in the thalamus predicted individual apathy severity across both patient groups and exhibited
256 y modulation by incentives was predictive of apathy severity, and independent of motor impairment and
259 ng recognition of the clinical importance of apathy, significant advances have been made in understan
260 ymptoms that occur in PD such as depression, apathy, sleep disorders (including rapid-eye movement sl
264 oup had significantly greater improvement in apathy than the placebo group at 4 weeks, 8 weeks, and 1
266 ontributes to continued misunderstanding and apathy toward fulfilling the regulatory and ethically ob
267 I scores (4.67 [3.21-6.78]), the presence of apathy (UPDRS item 4) (1.94 [1.33-2.82]), a higher levod
271 Exploratory LME models revealed that MBI-apathy was associated with higher CSF p-tau181 [6.03% (0
272 ed incentivisation by lower rewards, whereas apathy was associated with increased sensitivity to high
277 en that task performance in patients without apathy was no different to the age-matched control subje
278 contrast, above average improvement for mood/apathy was observed in the ventral border region of the
284 comparison, loss of goal-direct behaviour or apathy, was associated with changes in the direct pathwa
285 oural disturbance, including impulsivity and apathy, was associated with reduced functionally indepen
287 y clinical signs of parkinsonism, depression/apathy, weight loss, respiratory symptoms, mutations in
289 Depressed mood, anhedonia, anergia, and apathy were assessed at baseline using a structured beha
291 presenting clinically meaningful symptoms of apathy were compared with nonapathetic PD patients and h
294 ongest predictor of executive and initiation apathy, whereas functional indicators-particularly indep
295 stroke are depression, anxiety, fatigue, and apathy, which each occur in at least 30% of patients and
296 However, six patients endorsed increased apathy with half of the non-responders (e.g., less than
297 and 2, apathy without depression versus non-apathy without depression (80:26), disinhibition versus
298 pecific networks [combined Datasets 1 and 2, apathy without depression versus non-apathy without depr
299 alyses, seven core features were identified: apathy without moderate-severe dysphoria, behavioural di
300 ted symptoms and traits (e.g., anhedonia and apathy), yet no research has explored this issue transdi