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16. Ann Med Interne (Paris) 2000 Mar;151(2):97-106
[Olfactory disorders in Alzheimer's disease and in Parkinson's disease. Review of the literature].
[Article in French]
Nores JM, Biacabe B, Bonfils P
Service de Medecine Interne, Hopital Raymond-Poincare, Universite Paris V, Garches.
Olfactory disorders in Alzheimer's disease and Parkinson's disease have been the topic of a large body of work over the last decades. Work devoted to olfactory disorders in Alzheimer's disease includes over 300 papers providing clinical and fundamental data. Anatomy studies in Alzheimer's disease have demonstrated a specific concentration of lesions in peripheral and central olfactory structures (senile plaques, neurofibrillary degeneration) as well as lesions in layers II and III of the entorhinal cortex. These neuropathological findings led to the development of the hypothesis that olfactory disorders in Alzheimer's disease would result from a toxic process. Observed olfactory deficits involve both identification and recognition of odors and detection thresholds. Nevertheless, patients with Alzheimer's disease rarely consult for sensorial deficits as the other signs of the disease predominate. Neuropathology data on the olfactory system are much more sparse in Parkinson's disease. Lewy bodies suggestive of Parkinson's disease have been observed in the olfactory bulb and pathways, but, unlike Alzheimer's disease, the olfactory disorders appear to be stable, changing little over time, as opposed to the evolution of neurological symptoms and cognition impairment. Clinicians should be aware that olfactory disorders are an integral part of Alzheimer's disease and Parkinson's disease. Screening for sensorial impairment however is a secondary objective in the context of these neurodegenerative diseases.
17. J Neuropsychiatry Clin Neurosci 2000 Winter;12(1):29-33
Olfactory dysfunction discriminates probable Alzheimer's dementia from major depression: a cross-validation and extension.
McCaffrey RJ, Duff K, Solomon GS
University at Albany-State University of New York and Psychiatric Consultants, PC, USA.
The present study was conducted to cross-validate and extend the hypothesis that olfactory dysfunction could discriminate between groups of patients with Alzheimer's disease and major depression. Forty patients meeting the DSM-IV criteria for either Alzheimer's disease or major depression (20 per group) underwent assessment with the Pocket Smell Test (PST), a three-item screening measure of odor identification, and the Mini-Mental State Examination (MMSE). A PST score of < or = 1 (1 or 0 correct) discriminated between the groups with a hit rate of 97.5% (sensitivity = 95%, specificity = 100%). The optimal hit rate for the MMSE (< or =24) was less effective (hit rate = 90%, sensitivity = 80%, specificity = 100%). Age, gender, and education had minimal impact on the PST for both groups. Olfactory assessment continues to add to the diagnostic utility in the differential diagnosis of Alzheimer's disease versus major depression in elderly patients.
18. Neuropathol Appl Neurobiol 1999 Dec;25(6):481-91
beta-amyloid deposition and neurofibrillary tangle formation in the olfactory bulb in ageing and Alzheimer's disease.
Kovacs T, Cairns NJ, Lantos PL
Department of Neuropathology, Institute of Psychiatry, London, UK. tibor@neur.sote.hu
Impaired olfaction, hyposmia or anosmia are part of the clinical phenotype in neurodegenerative disorders including Alzheimer's disease (AD). It has been proposed that the most severely affected areas are interconnected with the central olfactory system in contrast to the relative sparing of other sensory areas which lack olfactory connections. The pathology of the first synaptic relay in the olfactory pathway, the olfactory bulb (OB), has been studied in AD, but the results have been inconsistent. In order to define more fully the pathology of the OB, we analyzed 15 AD and 15 control cases, using amyloid and tau immunohistochemistry on serial sections. This study demonstrates for the first time that all layers of the OB are severely affected in AD and in normal aging. The principal effector cells of the OB, the mitral cells, developed neurofibrillary tangles (NFTs) both in AD and in controls. All the cases, with the exception of two of the controls, contained NFTs. Amyloid immuno reactivity was detected in diffuse, primitive, classical and compact deposits in AD, while five control cases contained mainly diffuse deposits. We did not find a correlation between amyloid deposition and NFT formation. Among the control cases, two contained neither amyloid nor NFTs, eight had NFTs but no amyloid and only five had both NFTs and amyloid. All the AD cases had NFT and amyloid deposition. Our data suggest that the earlier pathology in the OB is NFT formation and more than ten NFTs/section is compatible with 93.3% diagnostic accuracy for AD.
19. Physiol Behav 1999 Apr;66(2):177-82
Loss of olfactory function in dementing disease.
Murphy C
University of California-San Diego, SDSU-UCSD Joint Doctoral Program in Clinical Psychology, 92120, USA. emurphy@sunstroke.sdsu.edu
Alzheimer's (AD) patients show neuropathological changes in areas of the brain central to olfactory processing, suggesting the theoretical importance and potential diagnostic utility of investigating functional changes in olfaction in these patients. Persons with Down's Syndrome who live to the fourth decade develop neuropathological changes in the brain similar to those found in AD. A series of investigations have been conducted to assess olfaction function in both patients with Alzheimer's disease and persons with Down's Syndrome. Functional testing included olfactory threshold, odor identification, odor similarity judgements, odor recognition memory, odor recall, odor fluency. Both Alzheimer's patients and persons with Down's Syndrome showed significant impairment in olfactory function, with some measures showing more impairment than others in the early stages of the disease process. Longitudinal investigation of several of the measures indicated decreased function over time consonant with falling DRS scores. Normal controls who tested positive for the APOE4 allele showed impaired odor identification compared to those who were allele negative. Patients with Huntington's Disease showed olfactory functional impairments, although the degree of impairment differed from the cortical dementias for some of these tasks. The sensitivity and specificity of these assessments will be discussed in relation to analogous assessments in other sensory modalities.
20. Int J Dev Neurosci 1998 Nov-Dec;16(7-8):777-85
Developmental and aging aspects of the cholinergic innervation of the olfactory bulb.
Durand M, Coronas V, Jourdan F, Quirion R
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
The olfactory bulb is a limbic paleocortex which receives monosynaptic sensory afferents from the olfactory mucosa, and a strong direct cholinergic input from the basal forebrain. This review focuses on the rat olfactory bulb as a suitable model to study cholinergic involvements in cortical processing, during development, adulthood and aging. Anatomical and biochemical data show that cholinergic influences upon the bulbar neuronal network are exerted through several types of target cells and receptors (muscarinic and nicotinic). Functional data indicate that cholinergic afferents to the olfactory bulb are involved in local events related to olfactory learning. Neurodegenerative disorders such as Alzheimer's disease involve early olfactory deficits and typical histopathological lesions in the olfactory bulb. In summary, with its exclusively extrinsic cholinergic innervation and direct sensory input, the rat olfactory bulb offers the opportunity to study the cellular and molecular mechanisms of cholinergic influences on cortical processing, in both normal and pathological conditions.
21. Neuropsychology 1999 Jan;13(1):47-53
Odor identification in normal aging and early Alzheimer's disease: effects of retrieval support.
Larsson M, Semb H, Winblad B, Amberla K, Wahlund LO, Backman L
Psychology Section, Stockholm Gerontology Research Center, Sweden.
Odor sensitivity and identification were examined in normal aging and early Alzheimer's disease (AD). The aims were to investigate AD as associated with lower odor sensitivity, odor identification as a function of retrieval support, and the relationship between global cognitive functioning (Mini-Mental State Exam [MMSE]; M. F. Folstein, S. E. Folstein, & P. R. McHugh, 1975) and olfactory performance. Results indicated intact odor sensitivity but deficient odor identification in AD. Both groups benefited from cues in identification, and the size of the gains was equally large in AD patients and controls. The finding of no selective benefit from retrieval support in AD suggests that a degradation of olfactory knowledge contributes to the odor identification deficits in these patients. MMSE and identification were positively related, whereas MMSE and olfactory sensitivity were unrelated. These findings suggest that the AD-related olfactory impairment stems from lesions in cortical rather than peripheral structures.
22. Ann N Y Acad Sci 1998 Nov 30;855:744-50
Apolipoprotein E status is associated with odor identification deficits in nondemented older persons.
Murphy C, Bacon AW, Bondi MW, Salmon DP
University of California, San Diego, La Jolla 92093-0957, USA. cmurphy@sunstroke.sdsu.edu
Alzheimer's
disease (AD) patients with moderate dementia show losses in olfactory
threshold, odor identification and odor memory. Sensitivity and specificity
of olfactory testing is significant, with the greatest power of accurate
diagnosis in the more cognitively loaded olfactory tasks. In patients
with very mild AD or in patients at risk for the disease because of
their mild cognitive impairment, losses are apparent for odor identification,
odor recognition memory and odor threshold, with the best sensitivity
in the identification task. Persons who are either heterozygous or
homozygous for the epsilon 4 allele of apolipoprotein E (ApoE) have
an increased risk of Alzheimer's disease, although they show no dementia
in the preclinical period. Evidence of olfactory dysfunction in this
population might be reflective of an incipient dementing process.
We have recently examined olfactory function in a group of normal
elderly persons who have undergone genetic testing for the Apoe4 allele.
These individuals consisted of all normal control subjects at the
University of California, San Diego (UCSD) Alzheimer's Disease Research
Center (ADRC) who had undergone both the genetic testing and testing
for olfactory function. All had been diagnosed as normal control participants
by two different neurologists who applied the National Institute of
Neurological Disorders and Stroke and the Alzheimer's Disease and
Related Disorders Association (NINDS-ADRDA) criteria for dementia.
Persons with a history of alcoholism, drug abuse, learning disability
or neurologic or psychiatric illness (including depression) were excluded.
In this population, persons with the Apoe4 allele showed significantly
poorer odor identification than those without an epsilon 4 allele.
Early appearance of olfactory deficits in the progression to AD in
persons with the epsilon 4 allele
suggests diagnostic utility in olfactory testing.
23. Ann N Y Acad Sci 1998 Nov 30;855:686-93
Odor memory in normal aging and Alzheimer's disease.
Nordin S, Murphy C
Department of Psychology, Umea University, Sweden. steven.nordin@psy.umu.se
The ability in normal elderly to verbally recall previously presented odors and to learn this task across trials was studied by applying a design which compared performance on the California Verbal Learning Test (CVLT) with an analogous odor test. Results suggest that both immediate and delayed recall of odors, both free and cued, as well as the ability to learn across trials is impaired in normal aging, perhaps more so for olfaction than for audition, which can be referred to poor use of semantic-clustering strategies and poor identification. Olfactory decline in memory in normal aging is, however, far from as affected as in Alzheimer's disease (AD). Two studies of persons with questionable AD demonstrated significant deficits in both recognition memory and identification of odors. Although further research is required, the findings from these 'pre-clinical' cases imply that performance on olfactory-mediated tasks may contribute to early diagnosis of AD.
24. Cereb Cortex 2000 Mar;10(3):243-51
Orbitofrontal cortex pathology in Alzheimer's disease.
Van Hoesen GW, Parvizi J, Chu CC
Department of Anatomy and Cell Biology, University of Iowa and Division of Cognitive Neuroscience, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242, USA. gary-van-hoesen@uiowa.edu
The orbitofrontal cortex has been examined in Alzheimer's disease (AD) from the viewpoint of neurofibrillary tangle (NFT) pathology, its laminar distribution and topography. NFT pathology in the orbitofrontal cortex is extensive in AD. In cases with extensive cortical pathology, NFTs extend from the pole of the frontal lobe to the orbitoinsular junction. In lesser affected cases, the anterior granular part of the orbital cortex is less invested by NFTs. Layers III and V contain the greatest density of NFTs and these are most dense in the dysgranular areas, posterior to the transverse orbital sulcus. Posterior and medial orbitofrontal areas, forming area 13 and the posterior tip of the paraolfactory gyrus, are the most severely damaged, as are the smaller agranular fields that surround the olfactory tract and cortex. The widespread orbitofrontal damage in AD affecting projection neurons suggests that this pathology may contribute heavily to the many non-memory-related behavior changes observed in this disorder.
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