Alzheimer’s disease (AD) is a progressive neurodegenerative disease, characterized by behavioral disorders, loss of memory and cognitive impairment affecting more than 48 millions worldwide. Cumulative evidence shows that innate immunity participates in the pathogenesis of AD. According with our neuroimmunomodulation hypothesis, microglial activation modifies the cross-talks between microglia and neurons. Thus, glial activation by the so called “damaged signals” triggers a cascade of pathological events leading to hyperphosphorylation and oligomerization of the tau protein, associated with cognitive impairment. This activation depends on the type and intensity of the stimulus. In AD, a persistently active microglial condition could generate neuronal damage and neurodegeneration favored by ApoE4, causing the release of pathological tau toward the extraneuronal environment. Released tau would subsequently cause reactivation of microglial cells, thus promoting a positive feedback and generating continuous cell damage. However, from the pathophysiological point of view, AD is significantly more complex that just inducing a loss of memory. As initial events in the pathogenesis of this neurodegenerative disease, alterations in the dopaminergic pathway together with serotonin depletion in the elderly lead to late onset depression according with recent evidences. These events seem to occur together with immunomodulatory alterations that lead to tau oligomerization in the course of neurofibrillary tangles formation. Interestingly, mood disorders are followed by neuroinflammatory processes and structural/functional alterations that lead to cognitive impairment in the context of AD (supported by Innova Corfo and the ICC).

There are many questions and conflicting research concerning the nature of the relationship between depression and dementia, i.e., are they coincidental, unidirectionally causal, mutually influencing or do they share a common pathophysiology.

Normal and pathological aging will be reviewed with a focus on the differences between crystallized and fluid intelligence. Effects of depression on cognition as individuals age are addressed.  Depression primarily impairs reaction time and some executive functions, such as mental flexibility, such that executive functions can appear impaired. There has been no demonstration of a consistent disturbance in memory functioning resulting from depression alone, whereas dementia is characterized by memory loss. Nonetheless memory complaints are ubiquitous amongst the elderly, regardless of whether they are healthy, depressed or dementing.

No consistent and agreed upon terminology is apparent throughout the literature on the relationship between dementia and depression, confounding a current understanding. For example, DSM-5 criteria for a diagnosis of depression may currently result in an under-reporting of major depression because elder patients tend demonstrate fewer symptoms and tend to focus on somatic and/or cognitive complaints rather than on mood issues. Thus, a nosology is proposed to help clarify these issues.

Depression confounds the diagnosis of dementia and vice versa. Current research has not provided a definitive understanding of this complex relationship. Recent studies have suggested that the magnitude and trajectory of depressive symptomatology have been underappreciated.

Perhaps the single greatest problem in understanding the relationship between dementia and depression is the heterogeneous nature of the illnesses themselves. Clarification can only come when careful specification of each group is made. In effect, apples must be compared with apples and not with oranges.

The intricacies of dementia are explored in relation to varied studies on brain atrophy in multiple sclerosis and used to delineate the primary pathology of the latter.
The theory examines the high frequency of cognitive impairment (Jongen 2012) in Multiple Sclerosis and its early manifestation during the disease.  The fact that there is associated brain atrophy cannot be explained by the degree of damage to neurons. (Carlos 2015) noted a 5 to 10 times greater rate of atrophy in Multiple Sclerosis.
The cognitive changes with Multiple Sclerosis are then correlated embryologically to the subependymal zone (Kazanis 2009) explaining the pathology of brain atrophy and why we have not made more progress through research.
Our understanding of the blood CSF barrier and the brain CSF interaction is poorly understood and probably holds the key to the symptoms of dementia (Erikson 2013). This interaction between the CSF and brain interstitial space is coordinated by the ependymal and subependymal zone of the brain. This is a novel concept that will aim to explain the links of all forms of dementia, as well as directing fertile areas for research.

Physical aging is widely accepted, and as a result, adaptive devices, tools and supports are implemented to compensate for physical challenges. Cognitive aging and dementia, on the other hand, tend to be stigmatized, with less awareness, understanding and acceptance. As a result, techniques and strategies to address both normal and abnormal cognitive aging are underutilized. The Amica approach to supporting cognitive well- being has a conceptual framework that applies to all Residents, whether they live in Independent living, Assisted Living or Memory Care. Through awareness, education and Team Member training, we maximize how Residents think, feel and function. Team Members receive extensive Amica-developed training in the areas of: 1) normal and abnormal cognitive aging, 2) personalization through Discovery, 3) a Cognitive Aging and Dementia Interactive experience (CADIE), and 4) a unique Behavior Support Program (BSP) that shares responsibility across all Team Members. Focusing on simple, effective and sustainable approaches, Residents live purposeful and meaningful lives with support that is balanced across multiple domains including an increased emphasis on goal attainment and psychological well-being. Empowering and supporting Residents to maximize potential is the goal. In this session the Amica Cognitive Well-Being Program will be shared with heightened emphasis on; 1) the culture change that was required, 2) multiple success stories, 3) the role and emphasis on neuroplasticity, and 4) general principles that can be utilized to benefit Residents living in any community, any environment, and anywhere along their cognitive journey.

Anyone who works in health care knows the reality of the statistics: the incidence of dementia is on the rise and the number of people living at home with later stages of the disease is also increasing. We are all hopeful for a cure, but what do we do in the meantime? This highly interactive and hands-on workshop will introduce renowned dementia care expert Teepa Snow’s Positive Approach to Care™ philosophy and associated care skills. These skills combine care techniques that match what is known about brain function changes through dementia, with the ability to complete dynamic assessment “in the moment” for all caregivers. Using these tools has been shown to reduce the incidence of responsive behaviours, which can delay institutionalization but more importantly, enhance quality of life both for people living with dementia and, also their formal and informal care partners. Additional benefits are increased efficiency and effectiveness by shifting focus from task-driven to patient-driven care.

At the end of the session, participants will have a toolkit of simple, practical, hands on skills that can be used immediately to aim for excellence in care. In the words of Teepa herself, “Until there’s a cure…there’s care.”

This talk is designed to help clinicians understand the evolution, detection, and clinical significance  of Mild Cognitive Disorder (MCI), which in DSM-5 is now termed Mild Neurocognitive Disorder (MiND). Beginning in the 1980’s the idea of a transitional stage between normal cognitive functioning in older adults and dementia began to be explored. Before that, mild cognitive symptoms were often attributed to depression or anxiety. The term MCI was first used by Reisberg and colleagues in 1988 to refer to Stage 3 on the Global Deterioration Scale. In addition, the Clinical Dementia Rating scale sought to identify early signs of dementia with an eye towards diagnosing dementia at the earliest point possible so has to maximize the efficacy of interventions. By 1999, the idea that MCI could be a prodrome or risk factor for further cognitive decline into dementia began to take hold. Initially, just as with the earlier DSM criteria for a diagnosis of dementia, early conceptions of MCI focused on the presence of memory impairments. Since these early conceptualizations, MCI has come to be associated with an acquired decline in one or more of six cognitive domains: attention, memory, language, visuospatial, executive function, or social cognition, in the context of independence in everyday day activities (i.e., complex instrumental activities of daily living). Compensatory behaviors are required to deal with this cognitive decline that is significant but not disabling.

Many elders note mild to moderate changes in cognitive functions and express concern about progression. In fact, memory complaints are ubiquitous amongst older adults. Concerns about memory or other cognitive faculties may lead an older adult to seek evaluation at this stage. Complicating accurate diagnosis is the fact cognitive symptoms often accompany psychiatric issues such as depression in older adults. Thus, an accurate diagnosis of MCI is critical to both rule out treatable causes of cognitive impairment and because MCI can represent the prodromal stage of major neurocognitive disorder, whether associated with Alzheimer’s disease or another etiology. MCI is the single best predictor of future dementia. Yet at the current time, even with the diagnostic criteria described in the DSM-5, the construct of MCI lacks clear operational clarity. While the addition of biomarkers to the diagnostic process is promising, they still require more investigation. At the current time the use of neuropsychological testing in the context of a multidisciplinary approach remains the most efficacious method to yield both an accurate diagnosis and a practical treatment plan.

Long-term research efforts on the action of single-molecule drugs on specific brain targets have proven their inefficiency for the treatment of Alzheimer´s disease (AD). Instead, the strategy of using natural compounds that tag several targets appears to be a promising solution to control the progress of this devastating disease. The latter strategy may face the need to rule out the presence of toxic molecules in the natural compounds. Therefore, an approach to use nutraceuticals with both acute and chronic toxicity assays and clinical trials on their effectivity is an attractive avenue. In this context, Evidence-based Nutraceutical Compounds (EBNC), containing bioactive molecules of demonstrated efficacy and biological security are opening solutions for a modern preventive medicine, and as potential solutions for AD. EBNC contain molecules of food supplements, that may exert pleotropic effects in controlling AD, and therefore can be used for the prevention or treatment of a disease. Their quality should be assured by rigorous processes of extraction from natural resources and GMP regulations. EBNC must exhibit sound preclinical studies and multicentric, double-blind, placebo-controlled clinical trials. These compounds are supported by major advances in genetics, epitranscriptomics and modern neuropharmacology, and are certainly opening a solid pathway toward the control of dementia.