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Introduction: Epidemiological studies have demonstrated that patients with diabetes mellitus have an increased risk of developing Alzheimer disease, but the relationship between the 2 entities is not clear. Development:Both diseases exhibit similar metabolic abnormalities: disordered glucose metabolism, abnormal insulin receptor signalling and insulin resistance, oxidative stress, and structural abnormalities in proteins and ␤-amyloid deposits. Different hypotheses have emerged from experimental work in the last two decades. One of the most comprehensive relates the microvascular damage in diabetic polyneuritis with the central nervous system changes occurring in Alzheimer disease. Another hypothesis considers that cognitive impairment in both diabetes and Alzheimer disease is linked to a state of systemic oxidative stress. Recently, attenuation of cognitive impairment and normalisation of values in biochemical markers for oxidative stress were found in patients with Alzheimer disease and concomitant diabetes. Antidiabetic drugs may have a beneficial effect on glycolysis and its end products, and on other metabolic alterations.ଝ Please cite this article as: Domínguez RO, Pagano MA, Marschoff ER, González SE, Repetto MG, Serra JA. Enfermedad de Alzheimer y deterioro cognitivo asociado a la diabetes mellitus de tipo 2: relaciones e hipótesis. Neurología.

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Among neurodegenerative diseases, Alzheimer’s disease (AD) is a leading cause of death in elderly individuals. AD is characterized, among other clinical findings, by unexplained weight loss, cachexia and altered immune function. To explore whether any relationship between gender and circulating levels of several eating-controlling metabolites exist, we evaluated leptin, tumor necrosis factor (TNF)-α, triiodothyronine (T₃), free (F) thyroxine (T₄), TSH, PRL, insulin (INS), and cortisol in 15 AD-treated patients (age range 55–82 years): 9 postmenopausal females (without hormone replacement therapy) and 6 males. The results (mean ± SEM) indicated that circulating leptin levels were significantly (p < 0.05) higher in female AD (40.34 ± 11.1 ng/ml) than in male AD (6.07 ± 1.39 ng/ml) patients. The difference found in circulating leptin levels was noticed regardless of BMI (26.75 ± 1.77 and 24.55 ± 1.93 kg/m², in females and males, respectively) and waist:hip ratios (0.91 ± 0.03 and 0.94 ± 0.02, in females and males, respectively). Moreover, serum TNF-α concentrations were also significantly (p < 0.02) higher in AD females (12.24 ± 1.47 pg/ml) than in AD males (6.62 ± 1.44 pg/ml), regardless of TNF-α:BMI ratios (0.50 ± 0.09 and 0.28 ± 0.08, in females and males, respectively; p > 0.05). Finally, no differences were observed between gender (in female and male AD patients, respectively) in circulating levels of T₃ (151.33 ± 9.91 vs. 116 ± 17.04 ng/dl), FT₄ (1.26 ± 0.08 vs. 1.24 ± 0.06 ng/dl), TSH (1.28 ± 0.16 vs. 2.46 ± 0.67 µIU/ml), PRL (10.53 ± 2.47 vs. 12.61 ± 2.37 ng/ml), INS (11.76 ± 1.95 vs. 8.59 ± 1.34 µIU/ml) and cortisol (15.71 ± 1.23 vs. 12.63 ± 1.47 µg/dl). These results indicate that our AD group of patients, with normal corticoadrenal and thyroid functions and normoprolactinemia, displayed a gender-related characteristic in the circulating levels of two very important anorectic signals, leptin and TNF-α, being both higher in female than in male AD patients, regardless of BMI. Our study suggests that increased circulating levels of both anorexigenic adipokines may contribute to the metabolic changes observed in AD females.

American trypanosomiasis (Chagas' disease), a zoonosis caused by Trypanosoma cruzi with a high incidence in Latin America, may induce an uncommon form of localized encephalitis termed "chagoma", found in few immunocompromised patients. The computed tomography (CT) and magnetic resonance imaging (MRI) findings of brain chagoma are reported for 3 males (ages 32, 32 and 9 yr), the first 2 infected with human immunodeficiency virus (HIV) and the third with acute lymphoblastic leukemia. Diagnosis was confirmed by biopsy. CT disclosed a single, supratentorial, nodular-shaped lesion that substantially enhanced with contrast material, localized in parietal or frontal lobes. T1-weighted MRI showed hypointense lesions that enhanced with gadolinium-diethylenetriaminepentaacetic acid, corresponding to extensive hyperintense areas on T2-weighted images, producing mass effect. The imaging pattern of brain chagoma presented here is similar to that of cerebral toxoplasmosis and should be considered in the differential diagnosis of an intracerebral mass lesion in immunocompromised patients.