Slide decks on Alzheimer’s disease:
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Alzheimer’s disease (AD) is a neurodegenerative disease that causes gradual cognitive decline and dementia. AD symptoms can be divided into three categories – cognitive, functional, and neuropsychiatric.
Cognitive symptoms in AD include memory, language, attention, visuospatial skills, and executive functions. Functional symptoms may be initially observed in work or social situations, progressing to problems with finances and self-care, eventually resulting in a complete loss of independent function for some individuals. Some neuropsychiatric symptoms (NPS) are key clinical manifestations of AD, with evidence that the prevalence of NPS increases with the severity of cognitive impairment. Particularly, symptoms of agitation, delusion, and irritability have been associated with worse cognitive performance.
The severity of cognitive impairment in people living with AD varies. Clinical diagnosis of cognitive impairment in individuals is essential for the individual’s overall care. There has been improvement in the level of awareness of dementia in primary care and specialist communities; however, increased awareness of the early signs of cognitive impairment within a clinical setting is still needed.
Get an introduction to what is currently known about AD by going through our slide decks. You can scroll through the slides, read the presenter notes or download the slides and use them for your own presentations and teaching.
Neurobiology and Aetiology
In the preclinical phase, the first measurable evidence of AD is an abnormal reduction in amyloid-beta1-42 levels within the CSF. Following this, amyloid-beta tracer retention is observed in PET scans, directly reflecting the build-up of amyloid. As AD progresses, neurodegeneration and synaptic dysfunction can be observed using structural and functional neuroimaging techniques. Go to the slide deck.
Course, Natural History and Prognosis
The staging method developed by Braak and Braak suggests that the neurofibrillary pathology of AD progresses in a relatively predictable sequence across the medial temporal lobe structures, subcortical nuclei, and neocortical areas of the brain in seven stages, with the final stage representing the absence of cortical neurofibrillary changes. Go to the slide deck.
Epidemiology and Burden
Due to the aging population, there is a growing number of people who are living with dementia due to AD or related conditions. In 2020, it was estimated that over 55 million people worldwide were living with dementia. The number of people affected is set to rise to 139 million by 2050, with the most significant increases in low- and middle-income countries. Go to the slide deck. Go to the slide deck.
Comorbidities are common in people living with AD where chronic comorbidities co-exist, such as diabetes and cardiovascular diseases. The relationship between comorbidity and AD is multifaceted, and causal relationships are difficult to disentangle. This slide deck describes current knowledge on the general medical and psychiatric comorbidities of AD. Go to the slide deck.
Treating AD involves managing multiple symptoms and minimizing long-term clinical deterioration. In this slide deck you will find basic concepts and definitions related to approaches such as disease-stage-specific treatment and psychosocial therapies. The slide deck also offers a brief introduction to general considerations for managing Alzheimer’s disease. Go to the slide deck.
Definitions and Diagnosis
Dementia is a degenerative and progressive brain disorder, characterized by the deterioration of cognitive function and commonly accompanied by a deterioration in emotional control, social behaviour or motivation. This deck explains dementia – its prevalence, signs, symptoms and diagnostic criteria. It is intended to provide an educational overview, complete with key definitions. Go to the slide deck.
Articles on Alzheimer’s Disease
Considerable advancements in AD research have been made over the years, working towards a reality of early identification with in-vivo biomarkers and multimodal treatment of patients with AD. Several disease-modifying therapies, such as agents targeting amyloid accumulation, tau pathology, and others, are being investigated.
Alzheimer’s disease causes gradual cognitive decline and dementia. Until recently, the definitive diagnosis of AD was based on autopsy assessments of brain amyloid-β plaques and tau neurofibrillary tangles, the defining biological features of AD. Biomarkers of amyloid-β and tau are vital for measuring AD pathology in living people and for differentiating between different neurodegenerative diseases. With the latest progress in AD research, accurate in-vivo diagnosis of AD is becoming increasingly crucial: before starting treatment with anti-amyloid therapies, it’s essential to determine if amyloid positivity is present. This article discusses AD biomarkers and their use in clinical and research settings and explore future research areas for wider clinical practice use.
Agitation is a frequent and distressing feature of advanced Alzheimer’s Disease and other dementias and its adequate management – non-pharmacological or pharmacological – is a major unmet need.
In familial disease associated with PSEN-1 mutations, symptomatic carriers show progressive loss of cortical thickness in areas involved in Alzheimer’s Disease. In contrast, in asymptomatic carriers increased thickness suggests that inflammatory processes or reactive neuronal hypertrophy may be involved in the preclinical phase. Further evidence of a non-linear trajectory in neuroanatomical changes comes from studies relating cortical thickness to beta-amyloid levels in CSF. The context for such studies is growing interest in diagnosing early stages of AD through biomarkers rather than clinical signs and symptoms.
Alzheimer’s disease is a form of dementia, characterised by gradual, progressive impairments in memory, reasoning, perception, and communication.
Images – free and ready to use
Download and utilize images illustrating pertinent aspects of Alzheimer’s disease. Selected images provide insights into high-performing CSF and plasma biomarkers summarizing Alzheimer’s disease diagnosis, brain metabolism PET imaging in Alzheimer’s disease, and Amyloid-PET imaging in Alzheimer’s disease.
PET tau across stages of Alzheimer’s disease
In vivo quantification of tau can be performed using tau-PET (PET: positron emission tomography). Tau-PET binds to insoluble neurofibrillary tangles, another core pathological feature of AD. Six stages that characterize tau pathology have been established through post-mortem studies1,2 and PET brain imaging.3 This illustration represents the stages of tau pathology measured by PET. Early stages are often accompanied by mild memory dysfunction; middle stages are accompanied by mild cognitive impairment; later stages are observed in individuals with AD dementia.
The figure is reprinted from Therriault J, et al. Nat Aging 2022;2(6):565–535. The content is licensed under a Creative Commons Attribution 4.0 International License. http://creativecommons.org/licenses/by/4.0/
3D Brain Atlas
Studies indicate that biological changes in the brain begin approximately two decades before the clinical onset of AD symptoms
- The staging method developed by Braak and Braak suggests that the neurofibrillary pathology of AD progresses in a relatively predictable sequence across the medial temporal lobe structures, subcortical nuclei, and neocortical areas of the brain in seven stages, with the final stage representing the presence of cortical neurofibrillary changes.
- In vivo neuroimaging data from neuropathological studies show a spatiotemporal development of Aß deposits in the brain, which originates in the cerebral regions and spreads from the neocortex, to the allocortex, to the brainstem, finally reaching the cerebellum.[2,3]