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25. Ann Otol Rhinol Laryngol 1998 May;107(5 Pt 1):421-6
Increased density of olfactory receptor neurons immunoreactive for apolipoprotein E in patients with Alzheimer's disease.
Yamagishi M, Getchell ML, Takami S, Getchell TV
Department of Surgery, Sanders-Brown Center on Aging, University of Kentucky College of Medicine, Lexington 40536-0230, USA.
Immunolocalization of apolipoprotein E (apoE) was investigated in human olfactory mucosa in which olfactory receptor neurons (ORNs) were identified with antiserum to protein gene product (PGP) 9.5. Tissue was obtained at autopsy from 10 nondemented middle-aged or elderly subjects and 9 patients with Alzheimer's disease (AD). Double-labeling immunofluorescence established that apoE immunoreactivity was colocalized in a subpopulation of PGP 9.5-immunoreactive ORNs. The mean number of apoE-immunoreactive ORNs per unit epithelial length in AD patients was about 3.5 times greater than that in nondemented patients, although the mean number of PGP 9.5-immunoreactive ORNs was similar. The apoE-immunopositive Schwann cells in olfactory nerve bundles were the probable source of apoE in the ORNs. The increased numbers of apoE-immunoreactive ORNs in AD patients compared to nondemented subjects demonstrates another manifestation of AD-related neuropathology, in addition to cytoskeletal changes, beta-amyloid deposition, and changes in immunoreactivity for other neuroproteins, that parallels changes in neurons in the AD brain.
26. Neuropsychol Rev 1998 Mar;8(1):11-23
Olfaction in persons with Alzheimer's disease.
Thompson MD, Knee K, Golden CJ
Center for Psychological Studies, Nova Southeastern University, Fort Lauderdale, Florida 33314, USA.
The need for low cost, noninvasive procedures for aiding in the diagnosis and understanding of Alzheimer's Disease (AD) has led to theories and procedures examining the role of olfactory disorders because of the finding that the brains of AD patients invariably exhibit neuropathology in the hippocampus and entorhinal cortex. This loss correlates with the increase in the number of plaques and tangles and with the severity of dementia. Considered together, these findings suggest that brain structures closely related to the olfactory system demonstrate significant histopathology in AD. A comprehensive review of the literature pertaining to olfaction in persons with AD revealed that the olfactory identification ability of patients with memory disorders is impaired relative to controls. Consistency is lacking, however, when olfactory detection thresholds are investigated. Also, there is inconsistency in regards to severity of illness and olfactory function. In addition to differentiating AD patients from normals, the olfactory paradigm has shown some limited usefulness in differentiating AD patients from some other demented patients.
27. J Neuropsychiatry Clin Neurosci 1998 Winter;10(1):64-7
Olfactory dysfunction discriminates Alzheimer's dementia from major depression.
Solomon GS, Petrie WM, Hart JR, Brackin HB
This study tested the hypothesis that olfactory dysfunction could discriminate between groups of patients with Alzheimer's disease and major depression. Forty patients meeting DSM-IV criteria for Alzheimer's disease and for major depression (20 per group) underwent assessment with the Pocket Smell Test (PST), a three-item screening measure of cranial nerve I function. A PST score of < or = 1 (1 or 0 correct) discriminated between the groups with a hit rate of 90% (sensitivity = 80%, specificity = 100%). Olfactory assessment may be a useful adjunctive screening measure in differentiating Alzheimer's disease from depression in elderly patients.
29.Prog Neurobiol 1997 Aug;52(6):511-35
The cholinergic system in Alzheimer's disease.
Kasa P, Rakonczay Z, Gulya K
Alzheimer's Disease Research Center, Albert Szent-Gyorgyi Medical University, Szeged, Hungary. kp@comser.szote.u-szeged.hu
The past decade has witnessed an enormous increase in our knowledge of the variety and complexity of neuropathological and neurochemical changes in Alzheimer's disease. Although the disease is characterized by multiple deficits of neurotransmitters in the brain, this overview emphasizes the structural and neurochemical localization of the elements of the acetylcholine system (choline acetyltransferase, acetylcholinesterase, and muscarinic and nicotinic acetylcholine receptors) in the non-demented brain and in Alzheimer's disease brain samples. The results demonstrate a great variation in the distribution of acetylcholinesterase, choline acetyltransferase, and the nicotinic and muscarinic acetylcholine receptors in the different brain areas, nuclei and subnuclei. When stratification is present in certain brain regions (olfactory bulb, cortex, hippocampus, etc.), differences can be detected as regards the laminar distribution of the elements of the acetylcholine system. Alzheimer's disease involves a substantial loss of the elements of the cholinergic system. There is evidence that the most affected areas include the cortex, the entorhinal area, the hippocampus, the ventral striatum and the basal part of the forebrain. Other brain areas are less affected. The fact that the acetylcholine system, which plays a significant role in the memory function, is seriously impaired in Alzheimer's disease has accelerated work on the development of new drugs for treatment of the disease of the 20th century.
30. Arch Neurol 1997 Aug;54(8):993-8
Olfactory dysfunction for pyridine and dementia progression in Alzheimer disease.
Nordin S, Almkvist O, Berglund B, Wahlund LO
Department of Psychology, Stockholm University, Sweden.
OBJECTIVE: To investigate whether odor detection sensitivity for pyridine, suggested by previous research not to be affected, is impaired in Alzheimer disease (AD) and whether an association exists between odor threshold and both degree of dementia and rate of dementia progression in AD. METHOD: The method of constant stimuli was used to determine odor thresholds for pyridine in 18 patients with AD (Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised and National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria) and 16 healthy elderly control subjects. All participants were carefully examined with medical and neuropsychological tests. RESULTS: Six patients with AD but none of the controls were anosmic (total olfactory loss) to pyridine, and the 12 nonanosmic patients had significantly higher detection thresholds (50% probability for detection, 323 parts per billion [ppb]) than did the controls (50% probability for detection, 105 ppb). In addition, an association was found between odor threshold and both degree of dementia and rate of dementia progression in AD. CONCLUSIONS: In contrast to previous findings, our results provide evidence that odor sensitivity in AD is impaired for pyridine. Odor sensitivity, in addition to other suggested predictors of progression rate, may be of interest for defining subgroups of AD or for clinical prognostic judgments of single patients.
31. Chem Senses 1997 Feb;22(1):105-10
Olfactory functions in Parkinson's disease and Alzheimer's disease.
Lehrner JP, Brucke T, Dal-Bianco P, Gatterer G, Kryspin-Exner I
University Clinic for Neurology, University of Vienna, Austria.
The aim of this investigation was to compare olfactory functions of patients suffering from Parkinson's disease (PD) and Alzheimer's disease (AD). Olfactory threshold, odor identification ability and odor memory performance were assessed in 21 non-demented PD patients and in 22 AD patients. Both patient groups were impaired in relation to an age-matched control group for the measure of odor identification. AD patients showed a higher olfactory threshold and poorer odor memory performance.
32. Psychiatry Clin Neurosci 1996 Feb;50(1):35-40
Olfactory evoked potentials in Parkinson's disease, Alzheimer's disease and anosmic patients.
Sakuma K, Nakashima K, Takahashi K
Division of Neurology, Faculty of Medicine, Tottori University, Yonago, Japan.
Olfactory evoked potential (OEP) recordings were undertaken using amyl acetate stimulation in 20 patients with Parkinson's disease, nine patients with Alzheimer's disease, seven patients with olfactory dysfunction with no other neurological disorder, and 17 control subjects. In order to eliminate the somatosensory factor from the combined somatosensory and olfactory components produced by amyl acetate stimulation, we substracted the potentials using odorless air from those using amyl acetate. In normal subjects, three components were observed, the mean latencies of which were 309 +/- 46, 484 +/- 61 and 710 +/- 55 ms. In all subjects with anosmia (n = 7), no responses were observed. In the patients with Alzheimer's disease, the components were fewer despite having no olfactory dysfunction. In the 20 patients with Parkinson's disease, eight [corrected] patients showed no components, seven patients showed one component and four [corrected] patients showed two components. The components rarely were detected in spite of whether the patients had olfactory dysfunction or not. Olfactory evoked potentials are useful in detecting olfactory dysfunction and the early stages of Alzheimer's disease and Parkinson's disease.
33. Life Sci 1996;59(5-6):491-8
Soluble beta-amyloid induces Alzheimer's disease features in human fibroblasts and in neuronal tissues.
Etcheberrigaray R, Payne JL, Alkon DL
Institute for Cognitive and Computational Sciences, Georgetown University Medical Center, Washington, DC, USA.
It has been shown that K+ channels, Cp20 (a 20kD GTP-binding protein), and intracellular calcium release, play a key role in associative memory storage. These same elements have been shown to be altered in fibroblasts from Alzheimer's Disease (AD) patients. In addition, it has been shown that PKC, also implicated in memory storage and closely related to the above mentioned components, is also altered in AD fibroblasts. Moreover, beta-amyloid was capable of inducing an AD-like phenotype for K+ channels and Cp20 in otherwise normal fibroblasts, providing additional evidence for the potential involvement of these components in AD and suggesting a possible pathological consequence of soluble beta-amyloid elevation in AD. Preliminary evidence shows that comparable changes in potassium channel function are also present in human olfactory neuroblasts from AD patients. These results indicate that the observed changes not only occur in peripheral tissues such as fibroblasts, but also in neural tissue, the primary site of AD pathology.
34. Percept Mot Skills 1994 Dec;79(3 Pt 1):1249-50
Anosmia in Alzheimer disease.
Solomon GS
Ten patients with probable Alzheimer Dementia underwent a brief evaluation of cranial nerve I function, with 90% showing varying degrees of anosmia. The potential usefulness of olfactory assessment in the evaluation of Alzheimer Disease is discussed.
35. Neurobiol Aging 1994 Nov-Dec;15(6):675-80
Protein alterations in olfactory neuroblasts from Alzheimer donors.
Johnson GS, Basaric-Keys J, Ghanbari HA, Lebovics RS, Lesch KP, Merril CR, Sunderland T, Wolozin B
Molecular Geriatrics Corp., Lake Bluff, IL 60044.
Definitive diagnosis of Alzheimer's disease (AD) is made by pathologic examination of postmortem brain tissue in conjunction with a clinical history of dementia. To date, there are no good biological markers for a positive diagnosis of AD in the living patient. In an effort to identify biological markers useful both in the clinical and pathologic diagnosis of AD, we have investigated disease-specific protein alterations in cultured olfactory neurons. Olfactory neurons are readily accessible by biopsy, can be propagated in primary cell culture as olfactory neuroblasts (ONs), and exhibit several elements of AD brain pathophysiology making them powerful tools for the study of AD. Two-dimensional gel analysis of ON proteins from neuropsychologically evaluated AD donors revealed a set of five proteins (Mr 17-50 kD, pI 4.8-6.7) that were significantly altered in concentration when compared to cells from age-matched controls. Further characterization and microsequence analysis could lead to the identification of proteins that may have important diagnostic or therapeutic value in the treatment of AD.
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