Type 2 diabetes and/or its treatment leads to less cognitive impairment in Alzheimer's disease patients.

Sirio-Libanés Hospital, Department of Neurology, School of Medicine, University of Buenos Aires (UBA), Buenos Aires, Argentina.
Diabetes research and clinical practice (Impact Factor: 2.74). 06/2012; 98(1):68-74. DOI: 10.1016/j.diabres.2012.05.013
Source: PubMed

ABSTRACT To evaluate the cognitive performance of a homogeneous population of Alzheimer's disease (AD), non-demented Type 2 Diabetes Mellitus (DIAB), demented with concomitant diseases (AD+DIAB) and healthy control subjects. AD is a progressive dementia disorder characterized clinically by impairment of memory, cognition and behavior. Recently, a major research interest in AD has been placed on early evaluation. Diabetes is one of the clinical conditions that represent the greatest risk of developing oxidative stress and dementia. Glucose overload, leading to the development of impaired-induced insulin secretion in DIAB and has been suggested to slow or deter AD pathogenesis.
The degree of cognitive impairment was determined on the Alzheimer Disease Assessment Scale-Cognitive (ADAS-Cog) and the Folstein's Mini Mental State Examination (MMSE); the severity of dementia was quantified applying the Clinical Dementia Rating (CDR) test; the Hamilton test was employed to evaluate depressive conditions; the final population studied was 101 subjects.
The cognitive deterioration is statistically significantly lower (p<0.05) in AD+DIAB patients as compared with AD patients.
In this longitudinal study the superimposed diabetic condition was associated with a lower rate of cognitive decline, while diabetic non-demented patients and controls present normal scores.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Studies on neurocognitive impairment among patients presenting with multi-infarct dementia (MID) have received little attention from non-Western societies, and the Arab world is no exception. To our knowledge, this is the first study to characterize neurocognitive, affective and vegetative functioning in patients with MID in Oman. Methods: In this study, we recruited 20 Omani patients presenting with MID and age- and gender-matched controls at the outpatient clinic of the Department of Behavioral Medicine, Sultan Qaboos University Hospital, Sultan Qaboos University, Muscat, Oman. In addition to the collection of clinical and demographic information, various cognitive batteries were administered to the consenting participants, including those indexing nonverbal reasoning abilities, working memory (attention, concentration and recall) and executive functioning. Questionnaires that elicit the affective range and the quality of sleep were also administered. Results: Compared with the matched healthy subjects, the patients diagnosed with MID significantly differed in the presently operationalized indices of visuospatial function, semantic memory and affective and vegetative functioning. In contrast, episodic memory and some attentional capacities were not significantly different compared with the control subjects. Conclusions: The present study was explorative and clinically designed to describe neurocognitive functioning in patients with MID seeking consultation at a tertiary care center in Oman. Our data are necessary for planning and setting up community services and health care programs for demented patients in a society where dementia is a growing silent epidemic.
    Dementia and Geriatric Cognitive Disorders Extra. 07/2014; 2014(4):271-282.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: Growing evidence supports the concept that insulin resistance plays an important role in the pathogenesis of cognitive impairment and neurodegeneration, including in Alzheimer's disease (AD). The metabolic hypothesis has led to the development and utilization of insulin- and insulin agonist-based treatments. Therapeutic challenges faced include the ability to provide effective treatments that do not require repeated injections and also the ability to minimize the potentially hazardous off-target effects. Areas covered: This review covers the role of intranasal insulin therapy for cognitive impairment and neurodegeneration, particularly AD. The literature reviewed focuses on data published within the past 5 years as this field is evolving rapidly. The review provides evidence that brain insulin resistance is an important and early abnormality in AD, and that increasing brain supply and utilization of insulin improves cognition and memory. Emphasis was placed on discussing outcomes of clinical trials and interpreting discordant results to clarify the benefits and limitations of intranasal insulin therapy. Expert opinion: Intranasal insulin therapy can efficiently and directly target the brain to support energy metabolism, myelin maintenance, cell survival and neuronal plasticity, which begin to fail in the early stages of neurodegeneration. Efforts must continue toward increasing the safety, efficacy and specificity of intranasal insulin therapy.
    Expert Opinion on Drug Delivery 11/2013; · 4.87 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Type 2 diabetes is a metabolic disease characterised by insulin resistance with hyperglycaemia and dyslipidaemia. It is associated with increased risk of stroke and vascular dementia, and might contribute to the development of Alzheimer's disease. Recent studies have shown that several antidiabetic drugs can promote neuronal survival and lead to a significant clinical improvement of memory and cognition in different clinical settings. We discuss these emerging data, with a focus on metformin, thiazolidinediones, and the more recently developed compounds targeting the glucagon-like peptide-1 receptor. Data show that these antidiabetic drugs affect brain metabolism, neuroinflammation, and regeneration. Evidence thus far strongly indicates that these antidiabetic drugs could be developed as disease-modifying therapies for human brain diseases in patients with and without diabetes.
    The lancet. Diabetes & endocrinology. 03/2014; 2(3):256-62.