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Abstract Background This study aims to review the methodologies used to identify the needs, the existing needs assessment instruments and the main topics of needs explored among caregivers of patients with mild cognitive impairment to dementia. Methods MEDLINE, PsycINFO, The Cochrane Library and Web of science were searched from January 1980 to January 2017. Research studies in English or French were eligible for inclusion if they fulfilled the following criteria: quantitative, qualitative and mixed method studies that used instrument, focus group or semi-structured interviews to assess the informal caregiver’s needs in terms of information, coping skills, support and service. Results Seventy studies (n = 39 quantitative studies, n = 25 qualitative studies and n = 6 mixed method studies) met the inclusion criteria and were included. Thirty-six quantitative instruments were identified but only one has been validated for the needs assessment of dementia caregivers: the Carer’s Needs Assessment for Dementia (CNA-D). The main areas of needs explored in these instruments were: information, psychosocial, social, psychoeducational and other needs. Conclusions No instrument has been developed and validated to assess the needs of informal caregivers of patients with cognitive impairment, whatever the stage and the etiology of the disease. As the perceived needs of caregivers may evolve with the progression of the disease and the dementia transition, their needs should be regularly assessed.

IntroductionA classification framework for posterior cortical atrophy (PCA) is proposed to improve the uniformity of definition of the syndrome in a variety of research settings.MethodsConsensus statements about PCA were developed through a detailed literature review, the formation of an international multidisciplinary working party which convened on four occasions, and a Web-based quantitative survey regarding symptom frequency and the conceptualization of PCA.ResultsA three-level classification framework for PCA is described comprising both syndrome- and disease-level descriptions. Classification level 1 (PCA) defines the core clinical, cognitive, and neuroimaging features and exclusion criteria of the clinico-radiological syndrome. Classification level 2 (PCA-pure, PCA-plus) establishes whether, in addition to the core PCA syndrome, the core features of any other neurodegenerative syndromes are present. Classification level 3 (PCA attributable to AD [PCA-AD], Lewy body disease [PCA-LBD], corticobasal degeneration [PCA-CBD], prion disease [PCA-prion]) provides a more formal determination of the underlying cause of the PCA syndrome, based on available pathophysiological biomarker evidence. The issue of additional syndrome-level descriptors is discussed in relation to the challenges of defining stages of syndrome severity and characterizing phenotypic heterogeneity within the PCA spectrum.DiscussionThere was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. The framework and terminology may facilitate the interpretation of research data across studies, be applicable across a broad range of research scenarios (e.g., behavioral interventions, pharmacological trials), and provide a foundation for future collaborative work.

White matter hyperintensities (WMH), frequently seen in older adults, are usually considered vascular lesions, and participate in the vascular contribution to cognitive impairment and dementia. However, emerging evidence highlights the heterogeneity of WMH pathophysiology, suggesting that non‐vascular mechanisms could also be involved, notably in Alzheimer's disease (AD). This led to the alternative hypothesis that in AD, part of WMH may be secondary to AD‐related processes. The current perspective brings together the arguments from different fields of research, including neuropathology, neuroimaging and fluid biomarkers, and genetics, in favor of this alternative hypothesis. Possible underlying mechanisms leading to AD‐related WMH, such as AD‐related neurodegeneration or neuroinflammation, are discussed, as well as implications for diagnostic criteria and management of AD. We finally discuss ways to test this hypothesis and remaining challenges. Acknowledging the heterogeneity of WMH and the existence of AD‐related WMH may improve personalized diagnosis and care of patients. [ABSTRACT FROM AUTHOR]

Introduction: Approximately 40% of dementia cases could be delayed or prevented acting on modifiable risk factors including hypertension. However, the mechanisms underlying the hypertension–dementia association are still poorly understood. Methods: We conducted a cross‐sectional analysis in 2048 patients from the MEMENTO cohort, a French multicenter clinic‐based study of outpatients with either isolated cognitive complaints or mild cognitive impairment. Exposure to hypertension was defined as a combination of high blood pressure (BP) status and antihypertensive treatment intake. Pathway associations were examined through structural equation modeling integrating extensive collection of neuroimaging biomarkers and clinical data. Results: Participants treated with high BP had significantly lower cognition compared to the others. This association was mediated by higher neurodegeneration and higher white matter hyperintensities load but not by Alzheimer's disease (AD) biomarkers. Discussion: These results highlight the importance of controlling hypertension for prevention of cognitive decline and offer new insights on mechanisms underlying the hypertension–dementia association. Highlights: Paths of hypertension–cognition association were assessed by structural equation models.The hypertension–cognition association is not mediated by Alzheimer's disease biomarkers.The hypertension–cognition association is mediated by neurodegeneration and leukoaraiosis.Lower cognition was limited to participants treated with uncontrolled blood pressure.Blood pressure control could contribute to promote healthier brain aging. [ABSTRACT FROM AUTHOR]

Introduction: Whether the reduction in brain amyloid beta (Aβ) plaque alone may substantially slow cognitive and functional decline in patients with dementia or mild cognitive impairment due to Alzheimer's disease (AD) remains debated. Methods: An instrumental variable meta‐analysis was performed to infer the effect of change in positron emission tomography (PET)–measured Aβ standardized uptake value ratio (SUVR) on cognitive and functional decline. Results: Pooling data from 16 randomized trials demonstrates that each 0.1‐unit decrease in PET Aβ SUVR is associated with a reduction (95% confidence interval) by 0.09 (0.034–0.15), 0.33 (0.12–0.55), and 0.13 (0.017–0.24) point in the average change of the Clinical Dementia Rating–Sum of Boxes, the Alzheimer's Disease Assessment Scale–Cognitive Subscale, and the Mini‐Mental State Examination, respectively. Discussion: This meta‐analysis provides statistically significant evidence of a likely causal relationship between a reduction in Aβ plaque and a reduction in cognitive and functional decline in patients with AD. Highlights: A widely cited meta‐analysis article concluded amyloid beta reduction does not substantially improve cognition.We identified data inconsistencies in the initial publication and found new trial data.We repeated the meta‐analysis after correcting data inconsistencies and adding new trial data.Updated results suggested statistically significant clinical benefit of amyloid beta reduction.Amyloid beta is a viable biological target for the treatment and prevention of AD. [ABSTRACT FROM AUTHOR]

Introduction: Global estimates on numbers of persons in early stages of Alzheimer's disease (AD), including prodromal and preclinical, are lacking, yet are needed to inform policy decisions on preventive measures and planning for future therapies targeting AD pathology. Methods: We synthesized the literature on prevalence across the AD continuum and derived a model estimating the number of persons, stratified by 5‐year age groups, sex, and disease stage (AD dementia, prodromal AD, and preclinical AD). Results: The global number of persons with AD dementia, prodromal AD, and preclinical AD were estimated at 32, 69, and 315 million, respectively. Together they constituted 416 million across the AD continuum, or 22% of all persons aged 50 and above. Discussion: Considering predementia stages, the number of persons with AD is much larger than conveyed in available literature. Our estimates are uncertain, especially for predementia stages in low‐ and middle‐income regions where biomarker studies are missing. [ABSTRACT FROM AUTHOR]