Alzheimer Disease: Persad C

Wright SL, Persad C. · Department of Psychiatry, University of Michigan Medical Center, Veterans Affairs Medical Center, GRECC, Ann Arbor, MI 48105, USA. · J Geriatr Psychiatry Neurol. · Pubmed #18004006 No free full text.

Abstract: Dementia and depression are frequently comorbid among older adult patients. Depression is related to cognitive decrement and can even represent the first signs of a neurodegenerative process. It can be difficult to distinguish depressed patients exhibiting the first signs of dementia from those whose cognition will improve with treatment. In this article, studies from the neuropsychological literature are reviewed that aid in accurate diagnosis and prognosis. Furthermore, the relationship between depression and dementia is explored by examining potential neurobiological mechanisms that may potentiate both syndromes in the context of the ongoing debate on depression as a prodrome and/or a risk factor for dementia. This article is concluded with suggestions for clinicians when deciding who to refer for neuropsychological assessment and with ideas for further research that might promote a better understanding of the complex association between depression and dementia during old age.

Gilman S, Koeppe RA, Little R, An H, Junck L, Giordani B, Persad C, Heumann M, Wernette K. · Department of Neurology, University of Michigan, Ann Arbor, MI 48109-0489, USA. · Exp Neurol. · Pubmed #15629765 No free full text.

Abstract: We compared the relative utility of neuropsychological testing and positron emission tomography (PET) with [18F]fluorodeoxyglucose ([18F]FDG) in differentiating Alzheimer's disease (AD) from dementia with Lewy bodies (DLB). We studied 25 patients with AD, 20 with DLB, and 19 normal elderly controls. There was no difference between patient groups for MMSE, confrontational naming, or verbal learning. The DLB group was significantly more impaired than the AD group for verbal fluency, and the AD group was significantly more impaired than the DLB group for verbal delayed recall. The DLB group had greater difficulty than the AD group on a visual discrimination task that does not require motor functioning, but the difference did not reach significance. Family ratings of motor functioning suggested significantly greater impairment in DLB patients than in AD patients. PET studies revealed significantly lower local cerebral metabolic rates for glucose (lCMRglc) for visual cortex (Brodmann areas 17, 18, and 19) in the DLB than the AD group, but no differences for other regions commonly affected in AD, including posterior cingulate, superior parietal lobe, lateral temporal lobe, and the prefrontal region. Motor ratings were significantly correlated with lCMRglc in all areas of cerebral cortex, including Brodmann areas 17, 18, and 19. The results demonstrate a similar profile of cerebral hypometabolism in the two patient groups except in the visual cortex, where the DLB group shows markedly lower lCMRglc than the AD group. Neuropsychological testing also differentiates the groups, and family ratings of motor functioning are as robust as PET in these later stages of the disorders.

Gilman S, Koeppe RA, Little R, An H, Junck L, Giordani B, Persad C, Heumann M, Wernette K. · Department of Neurology, University of Michigan, Ann Arbor, MI 48109-0316, USA. · Ann Neurol. · Pubmed #15174011 No free full text.

Abstract: We used positron emission tomography (PET) with (+)-[(11)C]dihydrotetrabenazine ([+]-[(11)C]DTBZ) to examine striatal monoaminergic presynaptic terminal density in 20 patients with dementia with Lewy bodies (DLB), 25 with Alzheimer's disease (AD), and 19 normal elderly controls. Six DLB patients developed parkinsonism at least 1 year before dementia (DLB/PD) and 14 developed dementia before parkinsonism or at about the same time (DLB/AD). Striatal mean binding potential was decreased by 62 to 77% in the DLB/PD group and 45 to 67% in the DLB/AD compared to AD and control. Binding was lower in the DLB/PD group than the DLB/AD, but the differences reached only marginal significance in the caudate nucleus. No differences were found between AD and control groups though a few AD patients had binding values below the range of the controls. Subsequent neuropathological examination in one AD patient revealed both AD and DLB changes despite the absence of clinical parkinsonism. Both DLB groups had an anterior to posterior binding deficit gradient relative to controls, largest in posterior putamen, smaller in anterior putamen, smallest in caudate nucleus. The DLB/AD group showed significant binding asymmetry only in posterior putamen. We conclude that PET with (+)-[(11)C]DTBZ differentiates DLB from AD, and decreased binding in AD may indicate subclinical DLB pathology in addition to AD pathology.