Alzheimer Disease: US Central Zone

Carrillo MC, Sanders CA, Katz RG. · Alzheimer's Association, Chicago, IL, USA. · Alzheimers Dement. · Pubmed #19362888 No free full text.

Abstract: The Alzheimer's Disease Neuroimaging Initiative is the largest public-private partnership on brain research underway at the National Institutes of Health. This 6-year study tracks cognitive and brain changes in normal subjects, those with mild cognitive impairment, and individuals with Alzheimer's disease. It was designed to provide better tools for performing effective clinical trials, and is slated to run until 2010. While data are being generated and analyzed, researchers involved in the study are developing an extension, i.e., the Alzheimer's Disease Neuroimaging Initiative II. The Foundation for the National Institutes of Health and the Alzheimer's Association convened a meeting to review the progress, evaluate future directions, and obtain the United States Food and Drug Administration's perspective on how the Alzheimer's Disease Neuroimaging Initiative could affect the drug-approval process.

Simpkins JW, Gatson JW, Wigginton JG. · Department of Pharmacology and Neuroscience, Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center, Fort Worth, TX, USA. · Alzheimers Dement. · Pubmed #19328446 No free full text.

This publication has no abstract.

Doody RS. · Effie Marie Cain Chair in Alzheimer's Disease Research, Baylor College of Medicine, Houston, TX, USA. · Alzheimers Dement. · Pubmed #19328443 No free full text.

Abstract: Despite enormous worldwide public and private interest in improving the prevention and treatment of Alzheimer's disease (AD), we have not made as much of an impact as we would like, and the number of affected individuals continues to grow. Even more alarmingly, whereas global efforts to identify AD cases and to develop new treatments are increasing, patient-care options are disappearing, so that even if a highly efficacious therapy or prevention approach arose, it would not be used effectively. As a first step toward organizing a better way forward, we should establish AD centers of excellence that mandate both patient care and research in the same setting. These centers would benefit from changes in public health policies related to chronic-disease surveillance, Center for Medicare and Medicaid Services funding for the care of chronic diseases, institutional review boards, good clinical practice guidelines, National Institutes of Health regulations for the use of research funds, Food and Drug Administration guidelines for the approval of AD drugs, and Department of Commerce regulations related to patent protection of AD diagnostic aids and treatments. This new form of AD centers of excellence would also provide direct care to many patients and their families, model care for communities and medical trainees, enhance the voluntary recruitment of AD patients to clinical trials, and improve our understanding of AD and its management.

Petersen RC. · Alzheimer's Disease Research Center, Mayo Clinic College of Medicine, Rochester, MN, USA. · Alzheimers Dement. · Pubmed #19328436 No free full text.

This publication has no abstract.

Weiner MF. · Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, USA. · Alzheimers Dement. · Pubmed #18631972 links to  free full text

Abstract: There are adequate scientific, public health, and ethical justifications for studying Alzheimer's disease (AD) in persons of varying race and ethnicity, but to be meaningful variables, race and ethnicity must be examined in context. The complex interactions between race, ethnicity, lifestyle, and environmental factors, such as climate and diet, require that future studies of AD in specific racial or ethnic groups attend to measures of racial/ethnic homogeneity and the assessment of the environment and the elements that comprise the ethnicity of groups under study. Instead of arbitrarily selecting specific racial or ethnic groups in the hope of finding important differences, it may be in the long run less costly and more efficient to recruit families with highly positive (or negative) family histories, to search within these groups for possible racial or ethnic differences, and to investigate the possible racial or ethnic reasons for those differences.

Griffin WS. · Geriatric Research, Education and Clinical Center, Neurobiology, Physiology, and Psychiatry, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA. · J Neuroinflammation. · Pubmed #18186919 links to  free full text

Abstract: Tumor necrosis factor-alpha (TNF) is one of a number of systemic and immunomodulating cytokines that generally act to promote acute-phase reactions but can drive degenerative changes when chronically elevated. Traditional focus on TNF has been directed at these inflammation-related functions. Of particular relevance to intersections between neuroinflammation and neurodegeneration is the ability of TNF to increase expression of interleukin-1 (IL-1), which in turn increases production of the precursors necessary for formation of amyloid plaques, neurofibrillary tangles, and Lewy bodies. More recent data have revealed that TNF, one of the few gliotransmitters, has strikingly acute effects on synaptic physiology. These complex influences on neural health suggest that manipulation of this cytokine might have important impacts on diseases characterized by glial activation, cytokine-mediated neuroinflammation, and synaptic dysfunction. Toward such manipulation in Alzheimer's disease, a six-month study was conducted with 15 probable-Alzheimer patients who were treated weekly with perispinal injection of Etanercept, an FDA-approved TNF inhibitor that is now widely used for treatment of rheumatoid arthritis and other systemic diseases associated with inflammation. The results demonstrated that perispinal administration of etanercept could provide sustained improvement in cognitive function for Alzheimer patients. Additionally, the authors were impressed by the striking rapidity with which these improvements occurred in the study patients. An example of this rapid improvement is presented in this issue as a case report by Tobinick and Gross. Such rapid gain of function inspires speculation about the role of gliotransmission or other equally rapid synaptic events in the relationship of TNF to Alzheimer-impacted neurophysiology. Because of the inability of large molecules such as etanercept to cross the blood brain barrier following conventional systemic administration, it is likely that the more direct drug delivery system pioneered by Tobinick also contributed to the effectiveness of the treatment. If so, this system could be useful in drug delivery to the brain in other neural disorders, as well as in animal research studies, many of which currently employ delivery strategies that inflict damage to neural cells and thus engender neuroinflammatory responses.

Bales KR. · Neuroscience Discovery Research, Eli Lilly & Co., Indianapolis, IN 46285, USA. · Exp Neurol. · Pubmed #17662278 No free full text.

This publication has no abstract.

Royall DR. · Division of Aging and Geriatric Psychiatry, The University of Texas, Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229-3900, Mail Code 7792, United States. · Neurobiol Aging. · Pubmed #17055613 No free full text.

This publication has no abstract.

Müller N. · Department of Communicative Disorders, University of Louisiana at Lafayette, LA 70504-3170, USA. · Clin Linguist Phon. · Pubmed #12945607 No free full text.

Abstract: Intelligibility is discussed in terms of the process of realizing a potential for mutual understanding, or intersubjectivity. The local management of mutual understanding, and its emergent properties within the context of an interaction are emphasized. Clinical applications of conceptualizing intelligibility as a potential rather than a property of speaker or interaction are discussed.

Holt J, Stiltner L, Wallace R, Raetz J. · Department of Family Medicine, Quillen College of Medicine, Eastern Tennessee State University, Johnson City, TN, USA. · J Fam Pract. · Pubmed #19508846 No free full text.

Abstract: Yes, but the extent of the benefit is unclear. Treating patients with early-stage Alzheimer's disease yields statistically significant, though perhaps not clinically significant, improvement in cognition and global function. In a few cases, it may delay loss of function and need for long-term care. Treating patients with mild cognitive impairment (MCI)-the most likely precursor to Alzheimer's disease-with cholinesterase inhibitors seems to have an initial, but perhaps unsustained, benefit over no treatment. Withdrawing anticholinergic drugs from patients taking them promises to reduce symptoms of MCI, but is unlikely to reduce rates of Alzheimer's.

Weintraub S, Salmon D, Mercaldo N, Ferris S, Graff-Radford NR, Chui H, Cummings J, DeCarli C, Foster NL, Galasko D, Peskind E, Dietrich W, Beekly DL, Kukull WA, Morris JC. · Cognitive Neurology and Alzheimer's Disease Center, Northwestern University Feinberg School of Medicine, 320 E. Superior, Searle 11-467, Chicago, IL 60611, USA. · Alzheimer Dis Assoc Disord. · Pubmed #19474567 No free full text.

Abstract: The neuropsychologic test battery from the Uniform Data Set (UDS) of the Alzheimer's Disease Centers (ADC) program of the National Institute on Aging consists of brief measures of attention, processing speed, executive function, episodic memory, and language. This paper describes development of the battery and preliminary data from the initial UDS evaluation of 3268 clinically cognitively normal men and women collected over the first 24 months of utilization. The subjects represent a sample of community-dwelling, individuals who volunteer for studies of cognitive aging. Subjects were considered "clinically cognitively normal" based on clinical assessment, including the Clinical Dementia Rating scale and the Functional Assessment Questionnaire. The results demonstrate performance on tests sensitive to cognitive aging and to the early stages of Alzheimer disease in a relatively well-educated sample. Regression models investigating the impact of age, education, and sex on test scores indicate that these variables will need to be incorporated in subsequent normative studies. Future plans include: (1) determining the psychometric properties of the battery; (2) establishing normative data, including norms for different ethnic minority groups; and (3) conducting longitudinal studies on cognitively normal subjects, individuals with mild cognitive impairment, and individuals with Alzheimer disease and other forms of dementia.

Herz J. · Department of Molecular Genetics, UT Southwestern, Dallas, Texas 75390-9046, USA. · Curr Opin Lipidol. · Pubmed #19433918 No free full text.

Abstract: PURPOSE OF REVIEW: Over the past few years, apolipoprotein E (ApoE) receptors, also known as LDL receptor-related proteins, have distinguished themselves as functionally diverse signaling receptors with pivotal roles not only in the vascular system but also in the nervous system and during development. RECENT FINDINGS: The expanding roles of ApoE receptors for cellular signal transduction at the same time transcend and integrate their lipid transport roles into a larger biological and clinical context. ApoE receptors are essential for the development of the nervous system, the regulation of synaptic plasticity, neuroprotection and the innervation of the muscle. They also regulate the metabolism of the amyloid precursor protein on multiple levels, implicating them in the pathogenesis of Alzheimer's disease. SUMMARY: ApoE, a common ligand for all members of the evolutionarily ancient LDL receptor gene family, is the major genetic modifier of the age of onset of Alzheimer's disease. The underlying molecular mechanisms remain shrouded in mystery, but the numerous critical functions of ApoE receptors within and outside the nervous system that have recently emerged make it likely that these multifunctional signal modulators participate in Alzheimer's disease pathogenesis. This review attempts to summarize the most recent and relevant findings in this area.

Smith DA. · Family Medicine, College of Medicine, Texas A&M University, College Station, TX, USA. · Am J Health Syst Pharm. · Pubmed #19420308 No free full text.

Abstract: PURPOSE: Pharmacologic treatment for patients with Alzheimer's disease (AD) who reside in long-term-care (LTC) facilities is discussed. SUMMARY: The recognition of AD can be problematic in patients residing in LTC who do not have a preexisting diagnosis of dementia. Residents in LTC facilities generally have fewer day-to-day cognitive demands, and, thus, nursing staff or caregivers may not recognize cognitive deficits until the disease is more advanced. The current therapeutic options for the treatment of AD are the cholinesterase inhibitors (ChEIs) and the N-methyl-d-aspartate receptor antagonist memantine. The ChEIs rivastigmine and galantamine are currently approved for the treatment of mild-to-moderate AD, and memantine is approved for the treatment of moderate-to-severe AD. The ChEI donepezil is presently approved for the treatment of mild, moderate, and severe AD in the United States. Two placebo-controlled trials in nursing-home patients receiving donepezil have been published. In both studies, donepezil appeared to be safe and effective for the treatment of AD in patients residing in LTC facilities. Data from an open-label study suggest that rivastigmine treatment might also provide benefits in nursing-home patients with moderate-to-severe AD. Another study demonstrated that treatment with galantamine might delay the need for transfer from an assisted-living facility to a nursing home. The effectiveness and safety of memantine have been assessed in a subgroup of patients with severe AD residing in LTC facilities. There were no major differences in safety and tolerability between the active treatment group and placebo. The relative and clinical importance of the cognitive, functional, and behavioral changes observed in LTC patients treated with ChEIs and memantine remain to be identified. CONCLUSION: Pharmacologic treatment should be recommended for most patients with AD who reside in LTC facilities.

Duysen EG, Li B, Lockridge O. · Researcher Eppley Institute, University of Nebraska Medical Center, Omaha, NE 68198 6805, USA. · Expert Opin Drug Metab Toxicol. · Pubmed #19416087 No free full text.

Abstract: Butyrylcholinesterase (BChE) mutations common in the human population may result in complete or partial BChE deficiency, making the BChE knockout (KO) mouse a model for human deficiencies. The BChE KO mouse cannot tolerate standard doses of the muscle relaxant succinylcholine or the Alzheimer's disease drugs huperzine A and donepezil. It is resistant to the asthma drug bambuterol. The importance of BChE in detoxication of cocaine has been demonstrated by hepatotoxicity and cardiotoxicity in cocaine-challenged BChE KO mice. The BChE KO mouse becomes obese on a high-fat diet, suggesting a role for BChE in fat metabolism. BChE serves as a backup for acetylcholinesterase by hydrolyzing the neurotransmitter acetylcholine in acetylcholinesterase knockout mice. Imaging studies show that BChE injected intrathecally crosses the blood-brain barrier. Mice, but not humans, have carboxylesterase in their blood. Carboxylesterase obscures the role of BChE in detoxication of organophosphorus pesticides. Future studies will make a double knockout that has neither BChE nor carboxylesterase. The double knockout is expected to be unusually sensitive to the toxicity of organophosphorus pesticides. Knowledge of drug sensitivities in the mouse model of human BChE deficiency will aid in understanding adverse drug effects in humans.

Maki PM, Dumas J. · Departments of Psychiatry and Psychology, Center for Cognitive Medicine, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60612, USA. · Semin Reprod Med. · Pubmed #19401956 No free full text.

Abstract: Use of estrogen therapy in the perimenopausal and postmenopausal periods has been shown in several clinical trials to help women maintain a premenopausal level of cognitive function. What is not yet fully understood is how the neurobiological effects of estrogen contribute to these cognitive effects. This review explores data from two related bodies of human literature that provide compelling evidence in support of the biological plausibility that estrogen treatment can benefit cognition. The first half of the literature review focuses on studies from the estrogen neuroimaging literature, and the second half focuses on pharmacologic challenge studies assessing estrogen-neurotransmitter interactions. We integrate these two bodies of literature by focusing on the neurophysiologic underpinnings of estrogen effects on cognition and linking these clinical studies to preclinical studies. The focus on verbal memory is important because it is a cognitive function that has been shown to change with estrogen treatment and predict Alzheimer's disease risk but is not addressed by preclinical studies. Overall, we conclude that estrogen interacts with cholinergic and serotonergic systems to affect hippocampal and frontal cortical brain areas and thereby enhance memory, particularly at the retrieval stage.

Jeitner TM, Pinto JT, Krasnikov BF, Horswill M, Cooper AJ. · Red Anvil, LLC, Milwaukee, Wisconsin, USA. · J Neurochem. · Pubmed #19393023 No free full text.

Abstract: Transglutaminases (TGs) are Ca2+-dependent enzymes that catalyze a variety of modifications of glutaminyl (Q) residues. In the brain, these modifications include the covalent attachment of a number of amine-bearing compounds, including lysyl (K) residues and polyamines, which serve to either regulate enzyme activity or attach the TG substrates to biological matrices. Aberrant TG activity is thought to contribute to Alzheimer disease, Parkinson disease, Huntington disease, and supranuclear palsy. Strategies designed to interfere with TG activity have some benefit in animal models of Huntington and Parkinson diseases. The following review summarizes the involvement of TGs in neurodegenerative diseases and discusses the possible use of selective inhibitors as therapeutic agents in these diseases.

Reddy VP, Zhu X, Perry G, Smith MA. · Department of Chemistry, Missouri University of Science and Technology, Rolla, MO 65409, USA. · J Alzheimers Dis. · Pubmed #19387111 No free full text.

Abstract: Oxidative stress plays a major role in diabetes as well as in Alzheimer's disease and other related neurological diseases. Intracellular oxidative stress arises due to the imbalance in the production of reactive oxygen/reactive nitrogen species and cellular antioxidant defense mechanisms. In turn, the excess reactive oxygen/reactive nitrogen species mediate the damage of proteins and nucleic acids, which have been shown to have direct and deleterious consequences in diabetes and Alzheimer's disease. Oxidative stress also contributes to the production of advanced glycation end products through glycoxidation and lipid peroxidation. The advanced glycation end products and lipid peroxidation products are ubiquitous to diabetes and Alzheimer's disease and serve as markers of disease progression in both disorders. Antioxidants and advanced glycation end products inhibitors, either induced endogenously or exogenously introduced, may counteract with the deleterious effects of the reactive oxygen/reactive nitrogen species and thereby, in prevention or treatment paradigms, attenuate or substantially delay the onset of these devastating pathologies.

Chen JY, Youn E, Mooney SD. · Informatics and Technology Complex (IT), Indiana University School of Informatics, IUPUI, Indianapolis, IN, USA. · Methods Mol Biol. · Pubmed #19381537 No free full text.

Abstract: Understanding how mutations lead to changes in protein function and/or protein interaction is critical to understanding the molecular causes of clinical phenotypes. In this method, we present a path toward integration of protein interaction data and mutation data and then demonstrate the identification of a subset of proteins and interactions that are important to a particular disease. We then build a statistical model of disease mutations in this disease-associated subset of proteins, and visualize these results. Using Alzheimer's disease (AD) as case implementation, we find that we are able to identify a subset of proteins involved in AD and discriminate disease-associated mutations from SNPs in these proteins with 83% accuracy. As the molecular causes of disease become more understood, models such as these will be useful for identifying candidate variants most likely to be causative.

Bassil N, Grossberg GT. · Division of Geriatric Medicine, St Louis University Health Sciences Center, St Louis, Missouri 63104, USA. · CNS Drugs. · Pubmed #19374459 No free full text.

Abstract: The mainstay of current management of patients with Alzheimer's disease involves drugs that provide symptomatic therapy. Research approaches for future therapy of Alzheimer's disease are focusing on disease modifying and/or preventive approaches. Two classes of medications have been approved by the US FDA for the treatment of Alzheimer's disease: the cholinesterase inhibitors (tacrine, donepezil, rivastigmine, galantamine), mostly for mild to moderate Alzheimer's disease, and the noncompetitive NMDA receptor antagonist memantine for the moderate to severe stages of Alzheimer's disease. Management of comorbid medical problems can be more complex in patients with dementia than in those without dementia. Unfortunately, medication adherence in Alzheimer's disease is low and good adherence is essential for attempting to slow disease progression and improve or stabilize quality of life. Simplifying treatment regimens and providing more caregiver- and patient-friendly modes of administration that fit in better with daily routines can ease caregiver stress which, in turn, may have a favourable impact on the patient's condition. To overcome problems of medication adherence in the elderly, simple, user-friendly dosage regimens should be prescribed for all medications; thus the need for novel regimens and delivery systems in the pharmacological treatment of Alzheimer's disease, such as once-daily donepezil, memantine and galantamine, and transdermal rivastigmine.

Tarawneh R, Holtzman DM. · Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. · CNS Neurol Disord Drug Targets. · Pubmed #19355934 No free full text.

Abstract: Over the last 10 years, promising data has emerged from both animal and human studies that both active immunization with amyloid-beta (Abeta) as well as passive immunization with anti-Abeta antibodies offer promise as therapies for Alzheimer's disease (AD). Data from animal models suggests that antibodies to Abeta through several mechanisms can decrease Abeta deposition, decrease Abeta -associated damage such as dystrophic neurite formation, and improve behavioral performance. Data from human studies suggests that active immunization can result in plaque clearance and that passive immunotherapy might result in slowing of cognitive decline. Despite this, a recent analysis from a phase I trial that involved active immunization with Abeta42, while not powered to determine efficacy, suggested no large effect of active immunization despite the fact that plaque clearance was very prominent in some subjects. An important issue to consider is when active or passive immunization targeting Abeta has the chance to be most effective. Clinico-pathological and biomarker studies have shown that in terms of the time course of AD, Abeta deposition probably begins about 10-15 years prior to symptom onset (preclinical AD) and that tau aggregation in tangles and in neurites does not begin to accelerate and build up in larger amounts in the neocortex until just prior to symptom onset. By the time the earliest clinical signs of AD emerge, Abeta deposition may be close to reaching its peak and tangle formation and neuronal cell loss is substantial though still not at its maximal extent. Since immunization targeting Abeta does not appear to have major effects on tangle pathology, for immunization to have the most chance for success, performing clinical trials in individuals who are cognitively only very mildly impaired or even in those with preclinical AD would likely offer a much better chance for success. Current work with AD biomarkers suggests that such individuals can now be identified and it seems likely that targeting this population with immunization strategies targeting Abeta would offer the best chance of success.

Bu G. · Hope Center for Neurological Disorders, Department of Pediatrics, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA. · Nat Rev Neurosci. · Pubmed #19339974 No free full text.

Abstract: The vast majority of Alzheimer's disease (AD) cases are late-onset and their development is probably influenced by both genetic and environmental risk factors. A strong genetic risk factor for late-onset AD is the presence of the epsilon4 allele of the apolipoprotein E (APOE) gene, which encodes a protein with crucial roles in cholesterol metabolism. There is mounting evidence that APOE4 contributes to AD pathogenesis by modulating the metabolism and aggregation of amyloid-beta peptide and by directly regulating brain lipid metabolism and synaptic functions through APOE receptors. Emerging knowledge of the contribution of APOE to the pathophysiology of AD presents new opportunities for AD therapy.

Paulsen JS, Duff K. · University of Iowa, Psychiatry Research, 1-305 Medical Education Building, Iowa City, IA 52242-1000, USA. · Neurology. · Pubmed #19332688 No free full text.

This publication has no abstract.

Carrillo MC, Blackwell A, Hampel H, Lindborg J, Sperling R, Schenk D, Sevigny JJ, Ferris S, Bennett DA, Craft S, Hsu T, Klunk W. · Alzheimer's Association, Chicago, IL, USA. · Alzheimers Dement. · Pubmed #19328456 No free full text.

Abstract: The purpose of the Alzheimer's Association Research Roundtable meeting was to discuss the potential of finding diagnostic tools to determine the earliest risk factors for Alzheimer's disease (AD). Currently, drugs approved for AD address symptoms which are generally manifest after the disease is already well-established, but there is a growing pipeline of drugs that may alter the underlying pathology and therefore slow or halt progression of the disease. As these drugs become available, it will become increasingly imperative that those at risk for AD be detected and possibly treated early, especially given recent indications that the disease process may start decades before the first clinical symptoms are recognized. Early detection must go hand-in-hand with qualified tools to determine the efficacy of drugs in people who may be asymptomatic or who have only very mild symptoms of the disease. Devising strategies and screening tools to identify and monitor those at risk in order to perform "prevention" trials is seen by many as a top public-health priority, made all the more urgent by an impending growth in the elderly population worldwide.

Yu F, Rose KM, Burgener SC, Cunningham C, Buettner LL, Beattie E, Bossen AL, Buckwalter KC, Fick DM, Fitzsimmons S, Kolanowski A, Janet K, Specht P, Richeson NE, Testad I, McKenzie SE. · University of Minnesota School of Nursing, Minneapolis, MN 55455, USA. · J Gerontol Nurs. · Pubmed #19326826 No free full text.

Abstract: The purpose of this article is to critically review and synthesize the literature on the effects of nonpharmacological cognitive training on dementia symptoms in early-stage Alzheimer's disease (AD) and related dementia. Electronic databases MEDLINE (PubMed), CINAHL, PsycInfo, and the Cochrane Library were searched using the keywords cognition, reality orientation, Alzheimer's disease, psychosocial factors, cognitive therapy, brain plasticity, enriched environments, and memory training. The findings support that cognitive training improves cognition, activities of daily living, and decision making. Interventions are more effective if they are structured and focus on specific known losses related to the AD pathological process and a person's residual ability, or are combined with cognitive-enhancing medications. Nursing implications are also discussed.

Specht JK, Taylor R, Bossen AL. · The John A. Hartford Center of Geriatric Nursing Excellence, The University of Iowa College of Nursing, Iowa City 52242-1121, USA. · J Gerontol Nurs. · Pubmed #19326825 No free full text.

Abstract: Evidence supports the maintenance of self-awareness in individuals with Alzheimer's disease (AD) and the individuals' ability to identify their own needs. The need for individualized, person-centered programming may be met only if the perceptions of the individuals with AD are taken into account and valued. There is strong support for individuals with AD to be involved in developing their plan of care. Plans should include supportive and educational programs, individualized to the person's self-identified needs. Plans must also take into account preserved self-awareness and address preservation of self-esteem, maintenance of abilities, management of behavioral symptoms including depression, and health promotion. Second author Richard Taylor, who has dementia, noted the absence of discussion on this joint planning in most of the AD literature. As he says, it omits the most important person, the person with dementia.