Abstract:A methodological approach to quality of life (QoL) assessment in Alzheimer's disease (AD) is challenging and few clinical trials have included it among outcomes, with conflicting results. In this review an indirect appraisal of evidence has been performed, searching the literature for the effect of drug treatments on determinants of QoL in AD. Among clinical factors associated with QoL, possible targets of drugs include cognition, which seems to be associated with QoL in early disease and can be positively affected by cholinesterase inhibitors (CIs) in this stage; functional decline, the risk of which can be decreased by CIs and memantine (MEM); behavioral and psychological symptoms, which can be reduced by MEM and atypical antipsychotics. Long-term observational studies have associated CIs and MEM treatment with a reduced institutionalization risk. According to the evidence, drug treatment of depression associated with AD should not be first choice from a QoL perspective, while treatment of pain can have beneficial effects on wellbeing indicators also in the late stages of the disease. Possible drug-related adverse events can affect QoL and should always be weighed against expected benefits from the patient's perspective. For this reason antipsychotic treatment is often problematic in AD and should be limited to severe psychosis and aggression, using the lowest effective doses for the shortest possible period. Conversely titration of CIs is necessary to reach the most effective dosages, although dose-related risk of adverse events has to be taken into account. Finally, CIs and MEM have been shown to reduce caregiver burden in randomized trials, possibly affecting caregivers' QoL.
Metabolic and neurodegenerative disorders have a growing prevalence in Western countries. Available epidemiologic and neurobiological evidences support the existence of a pathophysiological link between these conditions. Glucagon-like peptide 1 (GLP-1), whose activity is reduced in insulin resistance, has been implicated in central nervous system function, including cognition, synaptic plasticity, and neurogenesis. We review the experimental researches suggesting that GLP-1 dysfunction might be a mediating factor between Type 2 diabetes mellitus (T2DM) and neurodegeneration. Drug treatments enhancing GLP-1 activity hold out hope for treatment and prevention of Alzheimer's disease (AD) and cognitive decline.
Alzheimer's Disease (AD) is the most frequent form of dementia and represents one of the main causes of disability among older subjects. Up to now, the diagnosis of AD has been made according to clinical criteria. However, the use of such criteria does not allow an early diagnosis, as pathological alterations may be apparent many years before the clear-cut clinical picture. An early diagnosis is even more valuable to develop new treatments, potentially interfering with the pathogenetic process. During the last decade, several neuroimaging and cerebrospinal fluid (CSF) parameters have been introduced to allow an early and accurate detection of AD patients, and, recently, they have been included among research criteria for AD diagnosis. However, their use in clinical practice suffers from limitations both in accuracy and availability. The increasing amount of knowledge about peripheral biomarkers will possibly allow the future identification of reliable and easily available diagnostic tests.
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