As the number of patients with Alzheimer disease is expected to grow, finding ways to prevent and lower the risk of Alzheimer disease becomes a crucial matter. Risk factors for developing AD have been identified including health conditions, dietary habits, genetics and heredity, gender, education, age, and lifestyle. Interventions targeted at some of these risk factors may offer opportunities for development of an optimal preventive strategy. Life style habits which include dietary habits and physical activities appear to have positive effect on modifying many risk factors. Studies have shown controversial results when it comes to the relation between the adherence to a Mediterranean diet and /or physical activity and the incidence of Alzheimer disease. Many population-based studies reported the positive association between antioxidants intake (like Vitamin E and C), and polyunsaturated fatty acids whether it is from the diet or supplements on the cognitive performance. Future investigations should aim to determine objectively whether lifestyle modification through diet, exercise, or vitamins/supplements truly exert risk reduction or outright prevention. In this review, life-style habits are reviewed as they pertain to influence on risk of developing AD as well as on cognitive decline. Epidemiological studies and animal studies are reviewed.

There is an urgent need for new ways to treat Alzheimer’s disease (AD), the most common cause of dementia in the elderly. Current therapies are modestly effective at treating the symptoms, and do not significantly alter the course of the disease. Over the years, a range of epidemiological and experimental studies have demonstrated interactions between diabetes mellitus and AD. As both diseases are leading causes of morbidity and mortality in the elderly and are frequent co-morbid conditions, it has raised the possibility that treating diabetes might be effective in slowing AD. This is currently being attempted with drugs such as the insulin sensitizer rosiglitazone. These two diseases share many clinical and biochemical features, such as elevated oxidative stress, vascular dysfunction, amyloidogenesis and impaired glucose metabolism suggesting common pathogenic mechanisms. The main thrust of this review will be to explore the evidence from a pathological point of view to determine whether diabetes can cause or exacerbate AD. This was supported by a number of animal models of AD that have been shown to have enhanced pathology when diabetic conditions were induced. The one drawback in linking diabetes and insulin to AD has been the postmortem studies of diabetic brains demonstrating that AD pathology was not increased; in fact decreased pathology has often been reported. In addition, diabetes induces its own distinct features of neuropathology different from AD. There are common pathological features to be considered including vascular abnormalities, a major feature arising from diabetes; there is increasing evidence that vascular abnormalities can contribute to AD. The most important common mechanism between insulin-resistant (type II) diabetes and AD could be impaired insulin signaling; a form of toxic amyloid can damage neuronal insulin receptors and affect insulin signaling and cell survival. It has even been suggested that AD could be considered as “type 3 diabetes” since insulin can be produced in brain. Another common feature of diabetes and AD are increased advanced glycation endproduct-modified proteins are found in diabetes and in the AD brain; the receptor for advanced glycation endproducts plays a prominent role in both diseases. In addition, a major role for insulin degrading enzyme in the degradation of Aβ peptide has been identified. Although clinical trials of certain types of diabetic medications for treatment of AD have been conducted, further understanding the common pathological processes of diabetes and AD are needed to determine whether these diseases share common therapeutic targets.

Cardiac metastatic squamous cell laryngeal carcinoma is rare. We report the case of a 49-year-old man with recurrent squamous laryngeal carcinoma presenting with right leg acute ischaemia and large mobile right and left cardiac masses. The patient has history of laryngeal squamous cell cancer surgically treated with total laryngectomy, thyroidectomy, and tracheostomy 2 years ago. He was admitted to our intensive care unit with acute right leg pain, left sided chest pain, hypotension 92/55, and tachycardia 112 bpm. On physical exam, he had a faint pulse of his right Posterior Tibial artery with a cold foot, but no discoloration. Heart sounds were normal with no murmur. Initial workup showed a Troponin of 0.27. An electrocardiogram showed sinus tachycardia, with inverted T waves in the Infero-lateral leads. Emergent surgical thrombectomy was done on his right leg with restoration of arterial blood flow to the affected limb. An echocardiogram showed a preserved left ventricular function with multiple areas of echogenic masses in all four cardiac chambers located at the annulus of the tricuspid valve, the right ventricular free wall and along the inter-ventricular septum. No intracardiac shunt was detected by contrast study. Computed tomography scan of the heart confirmed the presence of multiple exophytic intracardiac masses within the left atrium, the right ventricle, interventricular septum, and lateral free wall of the left ventricle. Immunohistochemical staining with cytokeratin of the emboli was consistent with malignant squamous cell carcinoma consistent with metastases of his known laryngeal squamous cell cancer.

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