Severe dementia: A review on diagnoses, therapeutic management and ethical issues

Abstract North American data show that in the year 2000 around 4.5 million people had a diagnosis of dementia and more than a half were at moderate or severe stages of the disease. There is inevitable cognitive and functional decline caused by all etiologies of irreversible dementia as well as many behavioral symptoms that compromise the quality of life of both patients and caregivers. Few published studies have investigated issues concerning severe dementia such as predictors of mortality and life expectancy, nutrition, end of life issues and palliative care in terminal dementia, as well as best pharmacological and non-pharmacological treatments. Due to the complexity that characterizes advanced dementia, it is important that this discussion starts as early as possible allowing some decisions to be taken, preferably when the patients can still express their opinion

Active lifestyle enhances protein expression profile in subjects with Lewy body pathology.

Clinical trials of the effects of physical activity have reported improvements in symptoms and quality of life in patients with Parkinson's disease (PD). Additionally, morphological brain changes after exercising were reported in PD animal models. However, these lifestyle-related changes were not evaluated in postmortem brain tissue.ObjectiveWe aimed to evaluate, by immunohistochemistry, astrocytes, tyrosine hydroxylase (TH) and structural proteins expression (neurofilaments and microtubules - MAP2) changes in postmortem brain samples of individuals with Lewy body pathology.MethodsBraak PD stage≥III samples, classified by neuropathology analysis, from The Biobank for Aging Studies were classified into active (n=12) and non-active (n=12) groups, according to physical activity lifestyle, and paired by age, sex and Braak staging. Substantia nigra and basal ganglia were evaluated.ResultsGroups were not different in terms of age or gender and had similar PD neuropathological burden (p=1.00). We observed higher TH expression in the active group in the substantia nigra and the basal ganglia (p=0.04). Astrocytes was greater in the non-active subjects in the midbrain (p=0.03) and basal ganglia (p=0.0004). MAP2 levels were higher for non-active participants in the basal ganglia (p=0.003) and similar between groups in the substantia nigra (p=0.46). Neurofilament levels for non-active participants were higher in the substantia nigra (p=0.006) but not in the basal ganglia (p=0.24).ConclusionActive lifestyle seems to promote positive effects on brain by maintaining dopamine synthesis and structural protein expression in the nigrostriatal system and decrease astrogliosis in subjects with the same PD neuropathology burden

A review on shared clinical and molecular mechanisms between bipolar disorder and frontotemporal dementia

Mental disorders are highly prevalent and important causes of medical burden worldwide. Co-occurrence of neurological and psychiatric symptoms are observed among mental disorders, representing a challenge for their differential diagnosis. Psychiatrists and neurologists have faced challenges in diagnosing old adults presenting behavioral changes. This is the case for early frontotemporal dementia (FTD) and bipolar disorder. In its initial stages, FTD is characterized by behavioral or language disturbances in the absence of cognitive symptoms. Consequently, patients with the behavioral subtype of FTD (bv-FTD) can be initially misdiagnosed as having a psychiatric disorder, typically major depression disorder (MDD) or bipolar disorder (BD). Bipolar disorder is associated with a higher risk of dementia in older adults and with cognitive impairment, with a subset of patients presents a neuroprogressive pattern during the disease course. No mendelian mutations were identified in BD, whereas three major genetic causes of FTD have been identified. Clinical similarities between BD and bv-FTD raise the question whether common molecular pathways might explain shared clinical symptoms. Here, we reviewed existing data on clinical and molecular similarities between BD and FTD to propose biological pathways that can be further investigated as common or specific markers of BD and FTD

A review on shared clinical and biological aspects of bipolar disorder and frontotemporal dementia

Mental disorders are highly prevalent and important causes of medical burden worldwide. Co-occurrence of neurological and psychiatric symptoms are observed among mental disorders, representing a challenge for their differential diagnosis. Psychiatrists and neurologists have faced challenges in diagnosing older adults presenting behavioral changes. This is the case for early frontotemporal dementia (FTD) and late bipolar disorder. Early FTD is characterized by behavioral or language disturbances in the absence of cognitive symptoms. Consequently, patients with the behavioral subtype of FTD (bv-FTD) can be initially misdiagnosed as having a psychiatric disorder, typically depression or bipolar disorder (BD). Bipolar disorder is associated with a higher risk of dementia in older adults and cognitive impairment, where a subset of patients presents a neuroprogressive pattern during the disease course. Clinical similarities between BD and bv-FTD raise the question whether common molecular pathways might explain shared clinical symptoms. In fact, studies have also shown presence of molecular signatures related to bv-FTD in BD patients. Here, we reviewed existing data on clinical and molecular similarities between BD and FTD and propose biological pathways to be further investigated as common or specific markers of BD and FTD

A review on shared clinical and biological aspects of bipolar disorder and frontotemporal dementia

Mental disorders are highly prevalent and important causes of medical burden worldwide. Co-occurrence of neurological and psychiatric symptoms are observed among mental disorders, representing a challenge for their differential diagnosis. Psychiatrists and neurologists have faced challenges in diagnosing older adults presenting behavioral changes. This is the case for early frontotemporal dementia (FTD) and late bipolar disorder. Early FTD is characterized by behavioral or language disturbances in the absence of cognitive symptoms. Consequently, patients with the behavioral subtype of FTD (bv-FTD) can be initially misdiagnosed as having a psychiatric disorder, typically depression or bipolar disorder (BD). Bipolar disorder is associated with a higher risk of dementia in older adults and cognitive impairment, where a subset of patients presents a neuroprogressive pattern during the disease course. Clinical similarities between BD and bv-FTD raise the question whether common molecular pathways might explain shared clinical symptoms. In fact, studies have also shown presence of molecular signatures related to bv-FTD in BD patients. Here, we reviewed existing data on clinical and molecular similarities between BD and FTD and propose biological pathways to be further investigated as common or specific markers of BD and FTD