White matter microstructural abnormalities are increasingly found to be associated with cognitive impairment in Alzheimer’s Disease (AD). Here, we investigated the relationship between visual short-term memory (VSTM) performance, measured using a digital cognitive task, and integrity of brain white matter tracts. 52 AD and 60 age-matched healthy controls were recruited from the Oxford Cognitive Disorders Clinic. An established digital VSTM test – the Oxford Memory Task (OMT) – was used to measure several key memory metrics including: Identification Accuracy (percentage of correctly identified items), Target detection (probability of correctly identifying the target) and Misbinding (erroneously localizing an item to the remembered location of another item in memory). TBSS (Tract-Based Spatial Statistics) was then applied to investigate in which regions of the brain microstructural disruption of physiological diffusivity correlated with behavioural performance. A key common area, comprising the left optic radiation, forceps major and middle longitudinal fasciculus (MLF), was associated with performance across several VSTM metrics in patients with AD. In addition, misbinding was linked to the left MLF (part III), left inferior fronto-occipital fasciculus and left vertical occipital fasciculus. Microstructural disruption associated with target detection was additionally associated with superior longitudinal fasciculus, and Identification Accuracy with left superior thalamic radiation in AD. These findings reveal a common shared area of altered diffusivity in AD patients linked to global impairment in VSTM, while distinct types of memory errors are associated with disruption of additional contributions of selective white matter tracts. Key points ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This research was supported by funding from the Wellcome Trust (206330/Z/17/Z) and National Institute for Health and Care Research (NIHR) Oxford Health Biomedical Research Centre. Y.A.T. was supported by a PhD scholarship by the Friedrich-Ebert-Stiftung. I.M.I was supported by the University of Oxford and the University of Malaya. The funder played no role in study design, data collection, analysis and interpretation of data, or the writing of this manuscript. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Ethical approval was granted by the University of Oxford ethics committee (IRAS ID: 248379, Ethics Approval Reference: 18/SC/0448). I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes De-identified data supporting this study may be shared based on reasonable written requests to the corresponding author. Access to de-identified data will require a Data Access Agreement and IRB clearance, which will be considered by the institutions who provided the data for this research.

Deficits in visual short‐term memory (STM), rather than episodic long‐term memory, have recently been found to be associated with Alzheimer’s Disease (AD). However, the brain microstructural underpinning of selective abilities within visual STM remains poorly described.

Apathy is widely accepted to be a multidimensional syndrome. Assessment scales typically probe one or more dimensions but there is no consensus on the precise nature of these domains. Existing major theoretical frameworks include cognitive, behavioural, and emotional dimensions of apathy. While a social domain has also been suggested, it is far less well studied. Here we argue that although most assessment scales have been developed with these theoretical frameworks in mind, few findings actually support the existence of some of the dimensions that have been proposed, with the evidence for separation of cognitive and behavioural dimensions particularly lacking. In our opinion, although there is evidence for behavioural and emotional domains of apathy, the contention that there might be a separate dimension of cognitive or executive apathy is far less robust. Further, while there is some evidence for a social dimension of apathy, this has not been investigated sufficiently to make any definitive conclusion. We argue that there is a pressing need to reconsider different domains of apathy using robust analyses of proposed theoretical dimensions.

Apathy is a common, disabling neuropsychiatric syndrome that occurs across many brain disorders and may be associated with diminished motivation in behavioural, cognitive, emotional and social domains. Assessment is complicated by the variability of symptoms across apathy domains and self‐report from patients, which can be misleading due to their lack of insight. Independent evaluation by clinicians also has limitations though if it has to be performed with limited time. Caregiver reports are a viable alternative, but current assessments for them either do not distinguish between different apathy domains or are interview‐based and take long to administer. In this study, we developed a brief caregiver questionnaire version of the recently developed Apathy Motivation Index (AMI), which is a self‐report tool. We confirmed three apathy factors in this new caregiver measure (AMI‐CG) that were also present in the AMI: Behavioural Activation, Emotional Sensitivity and Social Motivation. Furthermore, we validated the scores against more extensive caregiver interviews using the established Lillle apathy rating scale as well as patient self‐reports of apathy, measures of depression, anhedonia, cognition, activities of daily living and caregiver burden across four different neurological conditions: Parkinson's disease, Alzheimer's disease, subjective cognitive impairment and limbic encephalitis. The AMI‐CG showed good internal reliability, external validity and diagnostic accuracy. It also uncovered cases of social apathy overlooked by traditional instruments. Crucially, patients who under‐rated their apathy compared to informants were more likely to have difficulties performing everyday activities and to be a greater burden to caregivers. The findings provide evidence for a multidimensional conceptualization of apathy and an instrument for efficient detection of apathy based on caregiver reports for use in clinical practice.