Antonio Cinturino

Tumor Diagnosis Preceding Alzheimer's Disease Onset: Is There a Link Between Cancer and Alzheimer's Disease?

Studies reporting an inverse association between Alzheimers disease (AD) and cancer are scant. Available data are mostly based on ancillary findings of mortality data or obtained from studies evaluating frequency of neoplasms in AD patients independently if they occurred before or after AD. Moreover, some studies estimated frequencies of neoplasms in demented individuals, who were not necessarily AD patients. We estimated frequency of tumors preceding the onset of AD in AD patients and compared it to that of age- and gender-matched AD-free individuals. Occurrence of tumors preceding AD onset was assessed through a semi-structured questionnaire. Tumors were categorized as benign, malignant, or of uncertain classification and as endocrine-related or not. Odds ratios (OR), used as measure of the association between the two diseases, were adjusted for tumor categories and known risk factors for AD and tumors. We included 126 AD patients and 252 matched controls. Tumor frequency before AD onset was 18.2% among cases and 24.2% among controls. There was a suggestive trend of an overall inverse association between the two diseases (adjusted OR 0.6; 95% CI 0.4-1.1; p = 0.11). Risk for neoplasms was significantly reduced only for women (adjusted OR, 0.5; 95% CI 0.3-0.9; p = 0.03) and for endocrine related tumors (adjusted OR, 0.5; 95% CI 0.2-1; p = 0.04). Our study confirms the inverse association reported in previous epidemiological studies. Though our findings might be explained by processes playing an opposite role in tumors development and neurodegeneration, they are also suggestive for a possible role of estrogen.

Frontal dementia related to thalamic stroke: a case report.

The behavioral variant of frontotemporal dementia (bvFTD) is characterized by modifications of personality, social behavior and cognition and relies on a neurodegenerative process [1]. However, vascular lesions affecting subcortical structures, mainly the caudate nucleus and thalamus, may result in a clinical syndrome resembling bvFTD [2, 3]. We report a case of paramedian thalamic stroke mimicking frontotemporal dementia. A 58-year-old righthanded man was referred to our hospital because of behavioral and cognitive changes formerly diagnosed as bvFTD. His medical history was negative for previous illness and the patient neither smoked nor drank alcohol. In July 2010, the patient suddenly presented with loss of consciousness and was admitted to a nearby hospital. After a few days the decreased level of consciousness resolved and he developed amnesia and personality changes such as disinhibition, apathy and loss of selfactivation. Toxicological exams, routine CSF analysis including total proteins, count cell, glucose and CSF culture were normal at admission. CT scan performed within twelve hours the onset of disturbances was also normal. The patient was diagnosed as affected by a conversion disorder. Because of the disturbances, the patient left his job and moved to live with his sister since he was not able to care for himself. After 6 months, the patient was submitted to a neuropsychological screening, showing an impairment of executive functions and amnesia. A diagnosis of frontotemporal dementia was supposed. The patient was referred to our Center in January 2011. The neurological examination was normal. Neuropsychological tests confirmed an alteration of executive functions as well as verbal and visual memory deficits. This was coupled with behavioral disturbances of apathy and depression. Brain MRI showed a mild frontotemporal atrophy with ventricular dilatation but also a left thalamic infarct in the paramedian territory (Fig. 1). The patient started therapy with paroxetine (20 mg/day) and memantine (10 mg/day). At 6-month and 1-year, follow-up neuropsychological test showed a further recovery of cognitive functions and behavioral disturbances (Table 1). The caregivers also reported a gradual improvement of disturbances since the onset. Brain CT confirmed thalamic infarction. We made a diagnosis of a thalamic stroke as the cause of dementia, because of the sudden onset and the gradual improvement of the clinical syndrome and the correspondent finding of an ischemic lesion. Routine blood tests, hemocoagulative screening and autoantibody pattern were normal. Electrocardiogram and carotid ultrasonography did not show any alterations. The transthoracic echocardiogram, the transcranial Doppler sonography and the transoesophageal echocardiography detected the patent foramen ovale (PFO) and the patient was started anticoagulant therapy. After 2 years, the S. Realmuto (&) V. Arnao A. Cinturino M. A. Mazzola S. Talamanca M. Riolo I. Cusmano C. Cupidi T. Piccoli Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche (BioNeC), Università degli Studi di Palermo, Via Gaetano La Loggia no 1, Palermo, Italy e-mail: sabrinarealmuto@gmail.com