Abstracts 49-60

Early Alert Alzheimers Home Screening Test

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Research Abstracts 49 - 60

Department of Pathology, Arthur M. Fishberg Center for Neurobiology, Mount Sinai Medical Center, New York, New York 10029.

In Alzheimer's disease, it has been recognized that there is a dramatic tendency for the development of neurofibrillary tangles among neurons of cortical regions associated with the olfactory system. We have demonstrated that neurofibrillary tangle-bearing neurons contain dramatically elevated levels of aluminum. The olfactory system, the only portion of the central nervous system with exposure to the external environment, is uniquely capable of uptake and transneuronal spread of exogenous substances. We argue that inasmuch as aluminum is not employed in any physiologic process, these deposits must arise from exogenous sources. Using parkinsonism-dementia complex of Guam as a model, we present data which suggest that the olfactory system is particularly vulnerable to damage and is affected very early in the disease. This supports the concept that etiologic agents of importance to this epidemic may be airborne in nature and may enter the central nervous system via the olfactory pathways.

Olfactory thresholds are associated with degree of dementia in Alzheimer's disease.

Recent neuroanatomical studies have noted that regions of the olfactory pathways contain high levels of neuritic plaques and neurofibrillary tangles, pathological hallmarks of Alzheimer's disease; and that the olfactory epithelium, the most peripheral level of the system, exhibits anatomical and biochemical changes in Alzheimer's disease. The present experiments investigated thresholds for olfactory and taste stimuli in patients with Probable Alzheimer's disease. Olfactory thresholds of Alzheimer's patients were significantly elevated relative to controls and were significantly correlated with scores on dementia scales. Taste thresholds of Alzheimer's patients were within normal limits and unrelated to scores on dementia scales. These results suggest that increased olfactory thresholds in patients with Alzheimer's disease reflect the effects of the disease process and, thus, may aid in the diagnosis and in the understanding of Alzheimer's disease.

Alzheimer's disease (AD) is considered to be the number one health problem and seems to be reaching epidemic proportion in the USA. The cause of AD is not known, a reliable animal model of the disease has not been found and appropriate treatment of this dementia is wanting. The present review focuses on the possibility that a virus or exogenous toxic materials may gain access to the CNS using the olfactory mucosa as a portal of entry. Anterograde and retrograde transport of the virus/zeolites to olfactory forebrain regions, which receive primary and secondary projections from the main olfactory bulb (MOB) and which, in turn, project centrifugal axons to the MOB, may initiate cell degeneration at such loci. Pathological changes may, thus, be initially confined to projecting and intrinsic neurons localized in cortical and subcortical olfactory structures; arguments are advanced which favor the view that excitotoxic phenomena could be mainly responsible for the overall degenerative picture. Neurotoxic activity may follow infection by the virus itself, be facilitated by loss of GABAergic terminals in olfactory cortex, develop following repeated episodes of physiological long term potentiation (which unmasks NMDA receptors) or be due to excessive release, faculty re-uptake or altered glutamate receptor sensitivity. Furthermore, a reduction in central inhibitory inputs to the MOB might then result in disinhibition of mitral/tufted neurons and enhance the excitotoxic phenomena in the MOB projecting field. Within this context, and in line with recent studies, it is believed that pathology begins at cortical (mainly olfactory) regions, basal forebrain neurons being secondarily affected due to retrograde degeneration. In addition, failure to produce a critical level of neurotrophic factors by a damaged MOB and olfactory cortex, could adversely affect survival of basal cholinergic neurons which innervate both regions. Support for these hypothesis is provided, first, by recent reports on pathological findings in AD brains which seem to involve preferentially the olfactory and entorhinal cortices, the olfactory amygdala and the hippocampus, all of which receive primary or secondary projections from the MOB; secondly, by the presence of severe olfactory deficits in the early stages of the disease, mainly of a discriminatory nature, which points to a malfunction of central olfactory structures.

Alzheimer's disease is a central nervous system disorder characterized by the presence of neurofibrillary tangles, neuritic plaques and dystrophic neurites in susceptible areas of the brain. Investigation of the mechanism and development of the disease has been hampered by the lack of an animal model and the inaccessibility of neural tissue during the illness. Deficits in odour detection and discrimination are among the signs of Alzheimer's and previous anatomical studies suggest that olfactory pathways may be involved early in the illness. Neurons in the olfactory epithelium, which are of central origin, are relatively accessible for biopsy and could be used as a source of living nerve cells for the study of Alzheimer's disease if they can be shown to have characteristics of this disease. As these neurons have the unusual property of arising from stem cells throughout the life of the organism, they are good candidates for the development of cell cultures or cell lines which may express the disorder from living patients. We report here that nasal epithelium tissue taken at autopsy shows unique pathological changes in morphology, distribution and immunoreactivity of neuronal structures in patients with Alzheimer's disease.

Olfactory detection and identification performance are dissociated in early Alzheimer's disease.

Ten carefully screened men with very mild symptoms of Alzheimer's disease (AD) and ten healthy controls of similar age were compared on multiple chemosensory tasks: odor detection and identification, and taste detection. The patients scored significantly worse than controls on identification of odors and of a subset of airborne stimuli providing trigeminal stimulation. In contrast, the patients' olfactory detection thresholds as well as taste detection thresholds were not impaired relative to those of controls. The patients' scores on neuropsychological tests and the results 18F-2 deoxy-D-glucose PET studies did not correlate with any of the chemosensory measures. The isolated odor identification deficit suggests that the initial chemosensory impairment in AD is central rather than peripheral.

The density and distribution of senile plaques and neurofibrillary tangles were examined in the olfactory bulbs and tracts, amygdala and hippocampus of 28 patients with Alzheimer's disease, 13 with Down's syndrome and 60 non-demented patients of age range 6-84 years. In all three patient groups comparisons of incidence and severity over the three areas showed the amygdala to be the most commonly and most severely affected area by senile plaques, the hippocampus by neurofibrillary tangles, and the olfactory bulbs and tracts to be the least affected by both. These findings are discussed in relationship to the possibility that the olfactory tracts might provide a portal of entry to the brain for any putative pathogenic agent(s) that might be responsible for the induction of senile plaques and/or neurofibrillary tangles.

Olfactory recognition: differential impairments in early and late Huntington's and Alzheimer's diseases.

Johns Hopkins University School of Medicine, Johns Hopkins Hospital, Baltimore, MD 21205.

Forty-two patients with senile dementia of the Alzheimer type (SDAT), 38 patients with Huntington's disease (HD) and matched normal controls were administered tests of olfactory, verbal, and visual recognition after being screened for normal olfactory discrimination. Early-affected Huntington's patients (EHD) with minimal chorea or cognitive deficit displayed marked deficits in olfactory recognition despite normal verbal and visual performance, even after correction for task difficulty, suggesting involvement of olfactory brain regions early in the disease process. In the early Alzheimer's group (EAD), marked deficits were seen on all recognition modalities indicating more global impairment. Both overall (early plus late) patient groups were impaired relative to controls on all recognition tasks, with the olfactory paradigm being most affected.

Many patients with dementia of the Alzheimer type (DAT) have an abnormal sense of smell. I studied 18 mildly demented subjects with DAT between the ages of 60 and 80 years and found them less able to identify five fragrances compared with 26 healthy elderly controls. The mean (+/- SEM) olfactory identification score for demented subjects was 0.3 +/- 0.2 compared with 2.8 +/- 0.2 for controls. When the subjects were given a multiple-choice list of ten items including the test fragrances and five other odors, performance of both demented and normal subjects improved, with a score of 1.8 +/- 0.4 for subjects with DAT and 4.2 +/- 0.2 for controls. The findings suggest that olfactory deficits are a sensitive, although non-specific, indicator of mild DAT.

Alzheimer's disease may begin in the nose and may be caused by aluminosilicates.

Genetic factors may interact with aging changes in the nasal mucociliary apparatus to increase the probability that ubiquitously occurring aluminosilicates may enter sensory neurons of the olfactory epithelium and spread transneuronally to several olfactory-related areas of the brain, thereby initiating changes that eventually result in neuronal damage typical of Alzheimer's disease. A speculative sequence of events is suggested by which neuronally-contained aluminosilicates might cleave or otherwise alter a normal cellular protein in such a manner that aggregates would arise that could interfere with cellular function and which also could act in a pseudo-infective manner, relaxing translational and transcriptional controls in the synthesis of the native protein. Some relevant experiments and potential therapies arising from the hypothesis presented are discussed.

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