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Introduction White matter hyperintensities (WMH) are often described in Alzheimer's disease (AD), but their topography and specific relationships with cognition remain unclear. Methods Regional WMH were estimated in 54 cognitively impaired amyloid beta-positive AD (Aβpos-AD), compared to 40 cognitively unimpaired amyloid beta-negative older controls (Aβneg-controls) matched for vascular risk factors. The cross-sectional association between regional WMH volume and cognition was assessed within each group, controlling for cerebral amyloid burden, global cortical atrophy, and hippocampal atrophy. Results WMH volume was larger in Aβpos-AD compared to Aβneg-controls in all regions, with the greatest changes in the splenium of the corpus callosum (S-CC). In Aβpos-AD patients, larger total and regional WMH volume, especially in the S-CC, was strongly associated with decreased cognition. Discussion WMH specifically contribute to lower cognition in AD, independently from amyloid deposition and atrophy. This study emphasizes the clinical relevance of WMH in AD, especially posterior WMH, and most notably S-CC WMH.

Cerebral amyloid angiopathy (CAA) is a common cerebrovascular disease involved in ischemic and hemorrhagic strokes, and its progression is correlated to cognitive decline. In vivo diagnosis of CAA is guided by the modified Boston criteria, with the presence of multiple intracerebral hemorrhage or cerebral microbleeds (CMB), or single hemorrhage and cortical superficial siderosis. The diagnosis of CAA is highly dependent on the quality of imaging and the advent of susceptibility-weighted imaging (SWI) sequences has improved sensitivity of MRI to detect hemosiderin deposition and CMB, hallmarks of CAA. We report here 3 clinical cases of patients with Alzheimer's disease and a focal form (i.e., not disseminated) of probable CAA, diagnosed with SWI sequences. Focal CAA may require closer attention and could offer keys in the understanding of both Alzheimer's disease and CAA pathogenesis.

We read the article by Therriault et al.,1 which highlights a frequency of biologically defined Alzheimer disease (AD) of 85.2% in patients with clinically defined AD and 7.88% in cognitively unimpaired individuals. The biological definition of AD leads to an increase in AD frequency as compared to a clinical definition2 because the biological definition of AD allows for the detection of disease in both symptomatic and asymptomatic individuals.2,3 A major issue is now to confirm that cognitive symptoms in patients with biologically defined AD with Alzheimer clinical syndrome are exclusively due to Alzheimer pathology and not associated with systemic factors, other brain diseases (e.g., vascular lesions, Lewy bodies, and TDP-43), or psychological comorbidities affecting attention. Indeed, if Alzheimer clinical syndrome is not restricted to Alzheimer pathology,4,5 and Alzheimer pathology is not rare in cognitively unimpaired individuals,1,2 there are probably patients with Alzheimer clinical syndrome and Alzheimer pathology in which this syndrome is not explained by this pathology. In these cases, AD is at a preclinical stage, and the clinical syndrome is secondary to other conditions. A better individual diagnosis would be an essential step forward in the field of individualized care for neurocognitive disorders.

Introduction Les troubles neurocognitifs (TNC) representent un enjeu majeur de sante public. Le diagnostic est souvent fait tardivement et la perception des enjeux ethiques du diagnostic semble differente selon les individus. Objectifs Determiner la perception des motivations et freins a realiser un diagnostic de TNC chez les medecins generalistes (MG), medecins specialistes (MS), autres professionnels de sante (P) et aidant informels (A). Methodes Une enquete nationale a ete realisee de juin a novembre 2016, adressee a ces 4 groupes evaluant leur perception de la pertinence des 8 principales motivations et des 8 principaux freins a realiser une demarche diagnostique de TNC, a quatre stades de la maladie : plainte cognitive isolee, TNC majeur aux stades leger, modere avec troubles psychocomportementaux et severe. La pertinence des concepts diagnostiques (diagnostic precoce, au moment opportun, personnalise) a ete evaluee. Resultats Parmi les 719 reponses (183 MG, 176 MS, 281 P et 79 A), plus de 90 % trouvaient pertinent de realiser un diagnostic sauf au stade severe (42,1 % a 70,9 %). Les motivations etaient superieures aux freins (p Discussion Les medecins (MG et SP) sont tres motives par la realisation d’une demarche diagnostique, mais cela diminue nettement au stade dementiel severe, contrairement aux A qui restent motives. Les MS percoivent beaucoup moins les freins que les MG, les P et les A, qui ont plus de proximite. Le diagnostic personnalise, avec elaboration d’un plan personnalise de soin est le plus pertinent. Conclusion Les motivations du diagnostic des TNC sont superieures aux freins, a tous les stades evolutifs, et le diagnostic personnalise est le concept diagnostic le plus pertinent.