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Background Dementia with Lewy body (DLB) is a common neurodegenerative disease that warrants specific care, which remains largely underdiagnosed. Our objective was to assess the knowledge of DLB by health professionals in comparison with that of Alzheimer's disease (AD), to better understand the reasons of its under-diagnosis. Methods We conducted a descriptive and analytical study processing the results of an online questionnaire submitted to French healthcare professionals between December 1, 2020 and March 1, 2021. Results A total of 490 healthcare professionals responded to the questionnaire. We observed a poorer knowledge of DLB compared to AD both subjective as highlighted on the self-assessment questionnaires and objective since the diagnostic criteria and therapeutic specificities were less known for DLB compared to AD. Conclusions DLB appears as a disease that is still too poorly known by health professionals. To improve training is therefore a decisive objective in order to optimize the therapeutic care and support of patients with DLB and their relatives.

Therapeutic perspectives in Alzheimer's disease. Alzheimer's disease (AD) is the most common cause of major neurocognitive disorders, affecting millions of people worldwide and leads to irreversible cognitive decline. The main neuropathological features of AD are the production of abnormal conformational protein (Amyloid Peptide, abnormally phosphorylated tau protein) leading to brain deposits, neuronal and synaptic loss and neurotransmitter deficiency including acetylcholine. The lesions occur 10 to 15 years before the first symptoms. The presence of specific markers in the cerebrospinal fluid is reflecting AD abnormalities (allow determining the presence of these abnormalities in living patients). Currently, only symptomatic treatments (acetylcholinesterase inhibitors and anti-glutamatergics) have been shown to be effective and have been marketed since the late 1990s. Since the early 2000s, therapeutic research has focused on the development of treatments that could modify the evolution of the disease either by increasing the elimination of abnormal proteins, or by decreasing their production and/or their diffusion into the brain. The two current targets are Aβ peptide and the abnormally phosphorylated Tau protein. Regarding the Aβ peptide, the therapeutic trials aimed at increasing its elimination were negative (ineffective) at the stage of major cognitive impairment but give hope for efficacy at the early stage of the disease. Therapeutic trials to reduce its production have been shown to be ineffective or deleterious to patients. Concerning the tau protein, the molecules under development aim at reducing its dissemination in the brain. Altogether, all potential disease modifying treatments are under development.Perspectives thérapeutiques dans la maladie d’alzheimer. La maladie d’Alzheimer est la cause la plus fréquente de troubles neurocognitifs majeurs, affectant des millions de personnes dans le monde et conduisant à un déclin cognitif irréversible. Les principales caractéristiques neuropathologiques de cette maladie sont la production de protéine de conformation anormale (peptide amyloïde, protéine tau anormalement phosphorylée) conduisant à des dépôts cérébraux, à une perte neuronale et synaptique et à un déficit en neurotransmetteur, notamment l’acétylcholine. Les lésions surviennent 10 à 15 ans avant les premiers symptômes, l’existence de marqueurs dans le liquide cérébrospinal spécifiques de la présence des anomalies de la maladie d’Alzheimer permettent de les objectiver chez les patients. Actuellement, seuls des traitements symptomatiques (inhibiteurs de l’acétylcholinestérase et antiglutamatergiques) ont démontré leur efficacité et sont commercialisés depuis la fin des années 1990. Depuis le début des années 2000, la recherche thérapeutique se concentre sur la modification des accumulations anormales en espérant modifier le cours évolutif de la maladie. Les essais thérapeutiques anti-Aβ visant à augmenter son élimination ont été négatifs (inefficaces) au stade d’altération cognitive majeure mais donnent un espoir d’efficacité à un stade plus précoce. Les essais thérapeutiques visant à diminuer sa production se sont révélés inefficaces ou délétères pour les patients. Les immunothérapies anti-tau en cours de développement ont pour objectif de diminuer sa dissémination dans le cerveau. Tous ces traitements potentiels sont encore en cours de développement.

Alzheimer's disease (AD) is the most common neurodegenerative disorder in older patients, leading to progressive cognitive impairment. Brain amyloid and tau deposits are the main pathological features of the disease and may appear several decades before the onset of clinical symptoms. The biomarkers of AD, measured in the plasma or in the cerebrospinal fluid, reflect the brain accumulation of beta-amyloid and tau. Therefore, they enable early and more accurate etiological diagnosis when combined with brain neuroimaging and neuropsychological assessment. The new definition of AD brings biomarkers forward, shifting the focus from symptoms to brain changes in living patients. The growing body of evidence from longitudinal studies has established their ability to improve the accuracy of AD diagnosis but also to predict the progression of cognitive impairment. The biomarkers of AD are also important for recruiting participants who are at increased risk of developing AD dementia in drug trials. Beyond their role in clinical research, these tools have been increasingly used for several years in clinical practice in secondary and tertiary-referral memory clinics. However, interpreting the results of AD biomarkers may be delicate in the oldest old patients with comorbidity. A tailored, patient-centered decision is mandatory in these situations. Complicated ethical issues may also arise in using these biomarkers in asymptomatic subjects. In the absence of clear guidelines for their utilization, we hereby discuss their potential interests and limitations in older adults.

The Alzheimer's disease (AD) is clinically characterized by the progressive appearance of amnesic disorders, which are followed by a clinical syndrome associating aphasia, apraxia and agnosia. In this picture are added behavioural problems, marked for example by decision-making or judgment confusions and disturbances of the orientation. The therapeutic perspectives are based especially on molecular targets that are the peptide Abeta, the protein tau or the facilitating molecular ways of neurodegeneration.