Ehab Tuppo

Stratford University, Stratford, Connecticut, United States

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Publications (3)9.06 Total impact

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    ABSTRACT: To determine the association between neuropsychiatric symptoms and the presence of medical illness among outpatients with mild dementia. The Neuropsychiatric Inventory (NPI) was used to assess neuropsychiatric symptoms, and the Cumulative Illness Rating Scale (CIRS) was used to evaluate physical impairment, in 44 outpatients diagnosed as having dementia (Alzheimer disease, n=22; vascular dementia, n=13; mixed dementia, n=9). The tests used were standard parts of a memory assessment program at a college of osteopathic medicine. Pearson product moment correlations were used to assess any associations between NPI and CIRS scores. Significant associations were identified between several NPI-assessed symptoms and degree of medical illness as measured by the CIRS. Neurobehavioral problems were significantly correlated (P<.05) with illness in the following body organ systems: gastrointestinal (lower), genitourinary, neurologic, ophthalmologic/otolaryngologic, psychiatric, and respiratory. The authors' preliminary data underscore the importance of primary care physicians assessing patients with dementia for comorbidity of psychiatric illnesses when conducting medical examinations.
    The Journal of the American Osteopathic Association 07/2006; 106(7):412-4.
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    Ehab E Tuppo · Hugo R Arias ·
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    ABSTRACT: Considerable evidence gained over the past decade has supported the conclusion that neuroinflammation is associated with Alzheimer's disease (AD) pathology. Inflammatory components related to AD neuroinflammation include brain cells such as microglia and astrocytes, the classic and alternate pathways of the complement system, the pentraxin acute-phase proteins, neuronal-type nicotinic acetylcholine receptors (AChRs), peroxisomal proliferators-activated receptors (PPARs), as well as cytokines and chemokines. Both the microglia and astrocytes have been shown to generate beta-amyloid protein (Abeta), one of the main pathologic features of AD. Abeta itself has been shown to act as a pro-inflammatory agent causing the activation of many of the inflammatory components. Further substantiation for the role of neuroinflammation in AD has come from studies that demonstrate patients who took non-steroidal anti-inflammatory drugs had a lower risk of AD than those who did not. These same results have led to increased interest in pursuing anti-inflammatory therapy for AD but with poor results. On the other hand, increasing amount of data suggest that AChRs and PPARs are involved in AD-induced neuroinflammation and in this regard, future therapy may focus on their specific targeting in the AD brain.
    The International Journal of Biochemistry & Cell Biology 03/2005; 37(2):289-305. DOI:10.1016/j.biocel.2004.07.009 · 4.05 Impact Factor

  • Neurobiology of Aging 07/2004; 25. DOI:10.1016/S0197-4580(04)81586-0 · 5.01 Impact Factor