Rates of disease progression differ among patients with Alzheimer's disease, but little is known about prognostic predictors. The aim of the study was to assess whether sociodemographic factors, disease severity and duration, and vascular factors are prognostic predictors of cognitive decline in Alzheimer's disease progression. We conducted a longitudinal clinical study in a specialized clinical unit for the diagnosis and treatment of dementia in Rome, Italy. A total of 154 persons with mild to moderate Alzheimer's disease consecutively admitted to the dementia unit were included. All patients underwent extensive clinical examination by a physician at admittance and all follow-ups. We evaluated the time-dependent probability of a worsening in cognitive performance corresponding to a 5-point decrease in Mini-Mental State Examination (MMSE) score.Survival analysis was used to analyze risk of faster disease progression in relation to age, education, severity and duration of the disease, family history of dementia, hypertension, hypercholesterolemia, and type 2 diabetes. Younger and more educated persons were more likely to have faster Alzheimer's disease progression. Vascular factors such as hypertension and hypercholesterolemia were not found to be significantly associated with disease progression. However, patients with diabetes had a 65% reduced risk of fast cognitive decline compared to Alzheimer patients without diabetes. Sociodemographic factors and diabetes predict disease progression in Alzheimer's disease. Our findings suggest a slower disease progression in Alzheimer's patients with diabetes. If confirmed, this result will contribute new insights into Alzheimer's disease pathogenesis and lead to relevant suggestions for disease treatment.

Patients with Alzheimer's disease (AD) have heterogeneous rates of disease progression. The aim of the current study is to investigate whether neuropsychiatric disturbances predict cognitive and functional disease progression in AD, according to failure theory. We longitudinally examined 177 memory-clinic AD outpatients (mean age = 73.1, SD = 8.1; 70.6% women). Neuropsychiatric disturbances at baseline were categorized into five syndromes. Patients were followed for up to two years to detect rapid disease progression defined as a loss of ≥ 1 abilities in Activities of Daily living (ADL) or a drop of ≥ 5 points on Mini-Mental State Examination (MMSE). Hazard ratios (HR) were calculated with Gompertz regression, adjusting for sociodemographics, baseline cognitive and functional status, and somatic comorbidities. Most patients (74.6%) exhibited one or more neuropsychiatric syndromes at baseline. The most common neuropsychiatric syndrome was Apathy (63.8%), followed by Affective (37.3%), Psychomotor (8.5%), Manic (7.9%), and Psychotic (5.6%) syndromes. The variance between the observed (Kaplen Meier) and predicted (Gompertz) decline for disease progression in cognition (0.30, CI = 0.26-0.35), was higher than the variance seen for functional decline (0.22, CI = 0.18-0.26). After multiple adjustment, patients with the Affective syndrome had an increased risk of functional decline (HR = 2.0; CI = 1.1-3.6), whereas the risk of cognitive decline was associated with the Manic (HR = 3.2, CI = 1.3-7.5) syndrome. In conclusion, specific neuropsychiatric syndromes are associated with functional and cognitive decline during the progression of AD, which may help with the long-term planning of care and treatment. These results highlight the importance of incorporating a thorough psychiatric examination in the evaluation of AD patients.

No abstract

Background/Aims: Visual deficits are frequent in Alzheimer’s disease (AD), yet little is known about the nature of these disturbances. The aim of the present study was to investigate color discrimination in patients with AD to determine whether impairment of this visual function is a cognitive or perceptive/sensory disturbance. Methods: A cross-sectional clinical study was conducted in a specialized dementia unit on 20 patients with mild/moderate AD and 21 age-matched normal controls. Color discrimination was measured by the Farnsworth-Munsell 100 hue test. Cognitive functioning was measured with the Mini-Mental State Examination (MMSE) and a comprehensive battery of neuropsychological tests. The scores obtained on the color discrimination test were compared between AD patients and controls adjusting for global and domain-specific cognitive performance. Results: Color discrimination performance was inversely related to MMSE score. AD patients had a higher number of errors in color discrimination than controls (mean ± SD total error score: 442.4 ± 84.5 vs. 304.1 ± 45.9). This trend persisted even after adjustment for MMSE score and cognitive performance on specific cognitive domains. Conclusions: A specific reduction of color discrimination capacity is present in AD patients. This deficit does not solely depend upon cognitive impairment, and involvement of the primary visual cortex and/or retinal ganglionar cells may be contributory.

Background: Alzheimer disease (AD) has heterogeneous clinical manifestations. Different neuropsychological profiles in AD patients might be indicative of the diffusion of the pathological process and might be associated with differences in rates of disease progression. Methods: We studied 154 newly diagnosed AD patients (65.6% women; mean age: 73 years). Performance in memory, executive functions, praxis and language domains was categorized into mild, moderate and severe impairment. The time-dependent probability of losing 5 points on the Mini-Mental State Examination (MMSE) over 2 years was considered as disease progression and evaluated by survival analysis. Results: One fourth of the patients decreased by ≧5 MMSE points over the 2-year follow-up. Rapid disease progression was more frequent in more educated patients and in those with moderate severity of global cognitive impairment. In univariate analysis, more severe memory and executive functioning impairment were associated with higher probabilities of progression. The association with memory was explained by differences in executive function impairment that remained statistically significant in multivariate analyses. Conclusions: Patients with more severe executive functioning impairment have a worse prognosis over 2 years. This might be due to involvement of the prefrontal cortex by the pathological process of AD in patients with severe executive deficits.

There are recent reports that alexithymia may be associated with brain dysfunction involving frontal lobes or right hemisphere regions. However, little is known about the relationship between alexithymia and cognitive deficits in Parkinson's disease (PD). The authors investigated the neuropsychological correlates of alexithymia in a population of 70 nondemented PD patients and 70 controls. Alexithymia was screened using the 20-item version of the Toronto Alexithymia Scale (TAS-20). Standardized scales that measure verbal episodic memory, executive functions, abstract reasoning, and visual-spatial and language abilities were adopted. PD patients with alexithymia performed worse than both PD patients without alexithymia and controls with or without alexithymia on tasks requiring visual-spatial processing. Moreover, regression analyses showed that, in PD patients, but not in controls, poor performance on a constructional praxis task predicted high scores on the TAS-20 subscale, which assesses difficulty in identifying emotions. These data evidence an association between alexithymia and visual-spatial processing alterations in PD patients, supporting the view that the right hemisphere could be specifically involved in the modulation of some facets of alexithymia.

No abstract

No abstract