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  • Reply to: When do we diagnose severe Alzheimer's disease?   1 month 3 weeks ago

    Dr. Salmeron's blog post above highlights some very important aspects of Alzheimer's Disease in a stage that devastates the lives of the patient and the caregivers and for a long time, was the stage where family members knew for certain that their loved one had dementia/Alzheimer's. For the past few decades’ awareness about AD has increased substantially and stages of cognitive impairment have been somewhat clearly delineated for mild and moderate AD. However, there is less clarity available for the designation of cognitive impairment as 'severe' or "advanced". This is the stage which requires the patient’s family to plan accordingly and timely assessment of function can provide accurate insight to the patient’s management team. There are two ways to characterize this change from moderate to severe: on a cognitive scale (such as MMSE or DRS) and on functional status (such as the Global Deterioration Scale or the Functional Assessment Staging). Dr. Salmeron's blog explains the advantages for these functional scales as this is the time when supervision and other changes are required to be made for the patient. It is important to understand the limitations of these functional scales as well. His short explanation does conclude that we should use both cognitive and functional scales to evaluate the patient in this late stage. The lack of tools to assess and manage this disease at this stage makes it very difficult for caregivers and providers. More research, suggested above, needs to focus on development of better care and management as well as awareness for severe AD.

  • Reply to: When do we diagnose severe Alzheimer's disease?   1 month 3 weeks ago

    Dr. Salmeron provides an excellent commentary regarding how best to diagnose patients with advanced AD. He correctly points out that most cognitive tests have floor effects that would preclude them from being useful while functional tests, which are generally administered less frequently, are probably more helpful. However, in advanced dementia, even functional scales may have limited utility given most patients with advanced dementia have no or very limited functional ability. Nevertheless, they are more sensitive than cognitive scales to subtle changes, particularly in patients with more advanced disease. Interestingly, behavioural symptoms often improve with progression from moderate to advanced dementia so may have limited utility. I myself find that certain cognitive scales, such as the severe impairment battery, which are sensitive to changes in social awareness, may be useful in helping to differentiate moderate from advanced dementia. The lack of valid and reliable tools highlights the need for future research in this area.

  • Reply to: When do we diagnose severe Alzheimer's disease?   1 month 3 weeks ago

    In the severe stage of Alzheimer's disease (AD), the cognitive and functional degeneration becomes accelerated. The common symptoms are the followings: 1) weight maintenance issues, 2) difficulty with eating and swallowing, 3) no bladder or bowel control, 4) considerable loss of memory, 5) gradual loss of speech and inability to say anything coherently, 6) inability to recognize once familiar surroundings and objects, 7) hallucinations, and 8) wander aimlessly [1].

    As AD enters the severe stage, independence is gradually lost and caregivers must provide consistent direct care with most if not all Basic Activities of Daily Living and Instrumental Activities of Daily Living. Safety issues and wandering require constant monitoring [2] and there is the need to create a safe environment [3, 4].

    In addition to DSM 5 and ICD-10, National Institute on Aging-Alzheimer's Association (NIAAA) criteria [5] are widely used to define severe AD. Moreover, another scale should be performed to define and manage AD patients in the severe stage. This scale is Neuropsychiatric Inventory (NPI) [6], based on a structured interview with a caregiver and/or patient’s relative. This scale is useful to assess the presence of neuropsychiatric symptoms in AD patients, and their impact on caregiver burden level. The NPI has shown stage-specific trends in neuropsychiatric symptoms in AD patients and has been demonstrated to be sensitive to drug treatment effects [7]. J. L. Cummings had written that the following neuropsychiatric abnormalities increase with dementia severity: delusions, agitation, dysphoria, anxiety, apathy, and aberrant motor behavior [8]. Disinhibition, indeed, seems to decrease with dementia severity [8].

    References
    [1] Alzheimerott (2015) Stages of Alzheimer’s disease. Available from: http://www.alzheimerott.org/stages-of-alzheimers-disease.php. Accessed November 24, 2016.
    [2] Futrell M, Melillo KD, Remington R, Schoenfelder DP (2010) Evidence-based guideline. Wandering. J Gerontol Nurs 36, 6–16.
    [3] Eshkoor SA, Hamid TA, Nudin SS, Mun CY (2014) A research on functional status, environmental conditions, and risk of falls in dementia. Int J Alzheimers Dis 2014, 769062.
    [4] Volicer L, van der Steen JT (2014) Outcome measures for dementia in the advanced stage and at the end of life. Adv Geriatr 2014, 346485. 
    [5] McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR Jr, Kawas CH, Klunk WE, Koroshetz WJ, Manly JJ, Mayeux R, Mohs RC, Morris JC, Rossor MN, Scheltens P, Carrillo MC, Thies B, Weintraub S, Phelps CH (2011) The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 7, 263–269.
    [6] Cummings JL, Mega M, Gray K, Rosenberg-Thompson S, Carusi DA, Gornbein J (1994) The Neuropsychiatric Inventory: comprehensive assessment of psychopathology in dementia. Neurology 44, 2308–2314.
    [7] Mega MS, Cummings JL, Fiorello T, Gornbein J (1996) The spectrum of behavior changes in Alzheimer's disease. Neurology 46, 130–135.
    [8] Cummings JL (1997) The Neuropsychiatric Inventory: assessing psychopathology in dementia patients. Neurology 48, S10-S16.

  • Reply to: Cognitive reserve in ageing and Alzheimer's disease.   1 month 3 weeks ago

    This article information is interesting because this review provides provides a discussion about the brain reserve and suggests.

  • Reply to: Protecting Progress   3 months 5 days ago
  • Reply to: I eat, therefore I am a nutrition expert   3 months 3 weeks ago

    We applaud the editorial “I eat, therefore I am a nutrition expert,”” by Martha Clare Morris.

    We have previously advanced the concern that clinical studies with nutritional interventions have an inherent compromise. Preclinical analyses with nutritional interventions have repeatedly demonstrated cognitive benefit, and have delayed the appearance of multiple Alzheimer-related biomarkers. Clinical studies with nutritional interventions, however, have typically been less successful. Part of this discrepancy is that preclinical studies allow a degree of control over basal diet (current and historical), environment/social interaction, age and genetic background that is virtually impossible to establish in clinical studies.

    Clinical nutritional studies are faced with the difficulty of recruiting sufficient numbers of individuals that have low or inadequate baseline nutritional status, such that a cohort with defined initiation of supplementation can be compared to an appropriate placebo cohort not receiving supplementation. An additional wrinkle arises in that while initiation of a nutritional intervention would at first thought be more likely foster improvement for individuals with a history of deficiency in the nutrient in question, these particular individuals may have undergo irreversible damage that may preclude any benefit. Any comprehensive attempt to address the full gamut of possibilities would therefore require cohorts of individuals with prior adequate diet, individuals with adequate diet plus whatever nutritional intervention is under consideration, and individuals with a prior deficient diet. These groups would then be further divided into groups that maintained their historical intake and those that altered their diet from deficient to adequate and vice versa. Finally, all of these cohorts would be independently randomized to receive the supplement or placebo, followed eventually by a crossover phase [1]. The complications inherent in clinical nutritional studies dramatically exceed those of pharmacological interventions, which have the inherent advantage that participants from diverse backgrounds are likely to have de novo exposure to the intervention.

    Effectively addressing even some of the above criteria in appropriately-controlled, randomized clinical nutritional studies, and monitoring what is by definition a complex outcome, warrants expertise far beyond that of those of us who can simply supplement the diet of one or more transgenic mice and monitor performance in maze trials or conduct histochemical analyses of a biomarker or two in brain tissue. The onset and progression of dementia is itself a grey area, and the impact of nutritional interventions is likely to extend the grey scale, rather than provide a black and white impact.

    Finally, consideration of the amounts of the supplement under investigation, and/or its precursors or metabolites, that may already be in the diet of some individuals, and the impact a one nutritional supplement on bioavailability of other nutrients, further call for nutritional expertise. In this regard, it is particularly noteworthy that combinatorial formulations, rather than individual vitamins or nutraceuticals, have displayed maximal impact [2].

    To carry the call for appropriate expertise raised by Dr. Morris one step further, we consider it essential that a clinical research team contain nurses and/or Physician’s Assistants for cognitive test administration and discussions with family members in order to optimize sensitivity and comfort of participants that is lost in the absence of one’s personal physician or neurologist.

    Thomas B. Shea
    Laboratory for Neuroscience
    UMass Lowell
    Lowell, MA 01854

    Ruth Remington
    Framingham State University
    Framingham, MA 07102

    REFERENCES
    [1] Shea TB, Rogers E, Remington R (2012) Nutrition and dementia: Are we asking the right questions? J Alzheimers Dis 30, 27-33.
    [2] Shea TB, Remington R (2015) Nutritional supplementation for Alzheimer’s disease. Curr Opin Psychiatry 28, 141-147.