Gut microbiota consists of over 100 trillion microorganisms including at least 1000 different species of bacteria and is crucially involved in physiological and pathophysiological processes occurring in the host. An imbalanced gastrointestinal ecosystem (dysbiosis) seems to be a contributor to the development and maintenance of several diseases, such as Alzheimer’s disease, depression, and type 2 diabetes mellitus. Interestingly, the three disorders are frequently associated as demonstrated by the high comorbidity rates. In this review, we introduce gut microbiota and its role in both normal and pathological processes; then, we discuss the importance of the gut-brain axis as well as the role of oxidative stress and inflammation as mediators of the pathological processes in which dysbiosis is involved. Specific sections pertain the role of the altered gut microbiota in the pathogenesis of Alzheimer’s disease, depression, and type 2 diabetes mellitus. The therapeutic implications of microbiota manipulation are briefly discussed. Finally, a conclusion comments on the possible role of dysbiosis as a common pathogenetic contributor (via oxidative stress and inflammation) shared by the three disorders.

Aim of this study was to investigate a) if through Magnetic Resonance Imaging (MRI) it was possible to reveal cerebral alterations in patients with insulin-dependent diabetes mellitus (IDDM); b) if there was any correlation with hypoglycemic episodes, glycometabolic control, microvascular alterations and diabetic peripheral neuropathy. For this purpose ten ID-DM patients under treatment with human insulin, aged 19-30 yr with the disease, the duration being from 1 to 19 yr, were investigated by MRI using a Philips Gyroscan. Spin Echo sequences were used with images in T1 T2 in sagittal and axial planes. To measure the ventricular dilatation the cerebroventricular index (CVI) was evaluated. The MRI has put in evidence in 7/10 patients a dilatation in the lateral ventricles and subarachnoidal spaces of the cerebral vault and the cerebellum clearly due to cerebral atrophy. The CVI mean values (34.78 +/- 2.92) were statistically (p < 0.001) higher in diabetic patients respect to control subjects (CVI mean values 27.5 +/- 1.58). These alterations did not present clear correlations with the degree of glycometabolic control, duration of disease, number of symptomatic hypoglycemic episodes and threshold for hypoglycemic symptoms, retinal microvascular alterations, microalbuminuria, diabetic peripheral neuropathy. The clinical or functional relevance of CVI changes and the exact pathogenic mechanism remains to be clarified.

Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder characterized by cognitive decline and by the presence of amyloid β plaques and neurofibrillary tangles in the brain. Despite recent advances in understanding its pathophysiological mechanisms, to date, there are no disease-modifying therapeutic options, to slow or halt the evolution of neurodegenerative processes in AD. Current pharmacological treatments only transiently mitigate the severity of symptoms, with modest or null overall improvement. Emerging evidence supports the concept that AD is affected by the impaired ability of the immune system to restrain the brain’s pathology. Deep understanding of the relationship between the nervous and the immune system may provide a novel arena to develop effective and safe drugs for AD treatment. Considering the crucial role of inflammatory/immune pathways in AD, here we discuss the current status of the immuno-oncological, immunomodulatory and anti-TNF-α drugs which are being used in preclinical studies or in ongoing clinical trials by means of the drug-repositioning approach.

The aim of this study was to determine the glycaemic indices (GIs), peak incremental indices (PI), and time of peak increment (TPI) of eight kinds of fruits and their relationship with the type and amount of simple sugars directly assayed in the fruits. Sixty-one type 2 diabetic patients randomized into eight groups--one for each category of fruit--participated in the study. GIs consisted of the following: pears = 60 +/- 4.9; apples = 63 +/- 8.3; oranges = 68 +/- 6.5; grapes = 70 +/- 7.5; plums = 75 +/- 8.4; peaches = 80 +/- 7.4; apricots = 82 +/- 9.1; bananas = 83 +/- 8.5. The PI values (mmol I-1) were the following: grapes = 2.52 +/- 0.26; apples = 3.13 +/- 0.75; pears = 3.48 +/- 0.55; oranges = 4.02 +/- 0.42; peaches = 4.07 +/- 0.38; apricots = 4.08 +/- 0.47; plums = 4.2 +/- 0.45; bananas = 4.45 +/- 0.39. There was no statistical differences in GI, and PI, within the different fruits. TPI of grapes (43.3 +/- 5.2 min), oranges (45 +/- 5.6 min), and peaches (45 +/- 5.6 min) were statistical different (p < 0.01) in respect to apricots (81.4 +/- 5.5 min). GIs were positively correlated with total glucose contained in the fruits (p < 0.05) and with PI (p < 0.0002); negatively with fructose both free (p < 0.02) and total (sum of free and present in sucrose (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)