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Early Alert Alzheimers Home Screening Test

Early Alert Home Screening Test is based on University of PA smell identification test which is considered to be the smell test equivalent to the eye chart. This test is simple, non-invasive, and self-administered.

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Research Abstracts 61- 72

The cortex of the superior temporal gyrus has been examined in two brains with Alzheimer's disease. Numerous neurofibrillary tangles and neuritic plaques that are characteristic of the disease, were present in area 38 in the anterior part of the gyrus and in area 22 more posteriorly but the primary auditory cortex, area 41, was virtually unaffected by these pathological changes. This relatively minor involvement of the primary auditory cortex, like that of the primary somatic and visual areas, again emphasizes the uniqueness of the olfactory system in being severely degenerate. The findings are considered to support the suggestion that the distribution of the pathological changes in Alzheimer's disease has an anatomical basis due to spread of the disease process along certain well-defined sets of cortical fibre connections.

Disturbances in the sense of smell may be important both clinically and theoretically in Alzheimer's disease. Initial evidence of poor olfactory recognition performance in Alzheimer's and parkinsonian dementias was followed by two reports which corroborated olfactory dysfunction in Alzheimer's disease. The neuroanatomical and neurochemical basis for this disturbance are discussed. Despite an abundance of preclinical and clinical data linking olfaction with acetylcholine, a preliminary study failed to show any effect of scopolamine on olfactory thresholds. Two of the olfaction-Alzheimer's studies found significantly better performance in other demented groups (alcoholics and patients with vascular dementia), suggesting possible utility in the differential diagnostic workup. The effect of aging per se on olfactory performance cannot be assessed without rigorous control for cognitive dysfunction in sampled populations.

Department of Otolaryngology, Mizonokuchi Hospital, Teikyo University School of Medicine, Kawasaki, Japan.

Characteristic changes that appear in the biopsied olfactory mucosa of patients with Alzheimer's disease (AD) were examined with immunohistochemical staining. Specimens were obtained from patients with clinical diagnoses of AD. Patients with vascular dementia and age-matched patients without dementia were used for controls. In most AD cases, neurofibrillary tangle-like abnormal tau protein (Tau) immunoreactivity was seen in the dendrites and perikarya of the olfactory receptor cells and in the nerve bundles. A senile plaque-like extracellular mass was found in the olfactory epithelium, and it reacted strongly to an anti-Tau antiserum and weakly to an anti-amyloid-beta protein antiserum. Ubiquitin (Ubq) immunoreactivity was also observed in the dendrites. Tau immunoreactivity of the perikarya and extracellular mass, and Ubq immunoreactivity were especially characteristic of the olfactory mucosa of AD patients. From these results, it is clear that the same pathologic changes in the brain are also present in the olfactory mucosa of patients with AD. Not only disruption of the central olfactory pathway, but also an olfactory disturbance of AD patients is caused by peripheral changes. Furthermore, an olfactory mucosal biopsy could be a useful method for a definitive diagnosis of AD.

A.E. Bennett Research Award 1993. Olfactory neuroblasts from Alzheimer donors: studies on APP processing and cell regulation.

Section of Geriatric Psychiatry, National Institutes of Mental Health, Bethesda, MD 20892.

Cell lines of continuously dividing human olfactory neuroblasts can be propagated using olfactory epithelium obtained from human donors at biopsy or autopsy. The expression of neuronal proteins in these cells, such as neurofilament protein and tau protein, can be increased using a combination of factors including nerve growth factor, fibroblast growth factor, interleukin 1 and interleukin 6. These cells also express aspects of human disease. Olfactory neuroblasts generated from donors with the common, sporadic forms of Alzheimer's disease, show elevated levels of the direct precursor to beta-amyloid, the amyloid precursor protein C-terminal derivative (CTD). When treated with the lysosomal inhibitor chloroquine, immunoblots of Alzheimer olfactory neuroblasts show seven-fold higher levels of CTDs than immunoblots from age-matched control neuroblasts. The disease related increases in CTDs can be reversed by treatment with agents that increase intracellular cyclic adenosine monophosphate (cAMP), such as dibutyryl-cyclic-AMP, theophylline, and isoproterenol.

College of Nursing, University of Arkansas for Medical Sciences, Little Rock 72205.

Although olfactory complaints prompt an estimated 200,000 people each year to seek medical consultation in the U.S., there is a dearth of information available in the nursing literature. Recent research links olfaction to degenerative processes in Alzheimer's disease, Parkinson's disease and human immunodeficiency virus infection. This article reviews anatomy and physiology of the olfactory system, describes alterations in smell function and reviews assessment with the University of Pennsylvania Smell Identification Test and odor detection threshold testing. Nurses can advocate thorough assessment and prompt treatment of associated conditions, and educate the patient and family regarding ways to maximize current functioning when olfaction is impaired.

Klinik und Poliklinik fur Hals-Nasen-Ohrenheilkunde, Universitatsklinikum Dresden.

Olfactory problems have deleterious consequences to systemic health, nutritional status and quality of life. Olfactory disorders are not as rare as generally assumed. Chemosensory dysfunction is most often secondary to one of only a few causes: nasal/sinus disease, viral infection, toxic chemical exposure, head trauma, as well as medication-related and idiopathic conditions. Many olfactory disorders are secondary to a wide variety of diseases, e.g. Alzheimer's disease. The patient's history may provide clues to these and other problems (e.g. toxin exposure, congenital dysosmia). Therapy should not begin until a standardized test has established the impairment of the sense of smell. Treatment of the underlying diseases may restore chemosensory function. The only truly reversible cause is inflammation, which is confirmed when smell returns after administration of corticosteroids. Reference is made to the need for adequate psychologic guidance of patients with chemosensorial problems. If restoration of their sense of smell is unlikely, patients should be educated to ensure safety in regard to such dangers as gas leaks, smoke, and spoiled foods.

The use of olfactory receptor neurons (ORNs) from biopsies to study changes in aging and neurodegenerative diseases.

Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104-3308, USA. rawson@pobox.upenn.edu

A gradual loss of olfactory capability with age and in a number of neurodegenerative diseases is common, and mechanisms underlying these losses are not understood. We determined the feasibility of using ORNs obtained from olfactory epithelial biopsies to identify possible changes in ORN function that may contribute to olfactory impairment in these individuals. ORNs from nine healthy subjects (66-84 yr), three patients with Alzheimer's disease and one with multi-infarct dementia were studied with calcium imaging techniques and two odorant mixtures. Seventy-five viable ORNs were studied; 53% of these were odorant responsive, and twenty percent of these responded to both odorant mixtures. In contrast, 25% of 173 ORNs from younger subjects were odorant responsive, and none of these responded to both odorant mixtures. The proportion of cells responding to each of the odorant mixtures also differed between older and younger subjects. These studies demonstrate the feasibility of this approach to examine age or disease-associated changes in neuronal function. Further, age-related changes in ORN selectivity may contribute to changes in olfactory performance.

Laboratory of Genetic Diseases Research, National Human Genome Research Institute, Bethesda, MD 20892-4472, USA. rlnuss@nhgri.nih.gov

For the past 40 years, research into Parkinson's disease (PD) has been predominantly the province of epidemiologists interested in pursuing the connection between the disease and environmental factors such as viral infection or neurotoxins. Hereditary influences were actually discounted because of a high monozygotic twin discordance rate found in studies that were later shown to be inadequate and inconclusive. There has recently been a resurgence of interest in investigating hereditary factors in PD when it became more and more apparent that a positive family history was a major risk factor for the disease. Meanwhile, it also became increasingly apparent from neuropathological studies that the common, idiopathic form of Parkinson's disease had, in fact, a pathological correlate, i.e., the existence of Lewy bodies, an eosinophilic cytoplasmic inclusion body, distributed diffusely throughout the substantia nigra, hypothalamus, hippocampus, autonomic ganglia and olfactory tracts. Although candidate gene approaches to linkage in PD families have not been rewarding, a genome wide scan mapped PD to 4q21-23 in one large family with PD with diffuse Lewy bodies, where a candidate gene, alpha-synuclein, resides. This gene encodes a presynaptic protein of which a peptide fragment is known to be a constituent of Alzheimer's disease plaques. The identification of a missense mutation in the alpha-synuclein gene in four independent PD families suggests that at least some fraction of familial PD with diffuse Lewy bodies is the result of an abnormal protein that interferes with normal protein degradation leading to the development of inclusions and ultimately neuronal cell death. There may be common pathogenetic mechanisms involved in alpha-synuclein mutations in PD and beta-amyloid and presenilin gene mutations in Alzheimer's disease.

Klinik und Poliklinik fur Hals-Nasen-Ohren-Heilkunde der Medizinischen Fakultat Carl Gustav Carus, Technischen Universitat Dresden.

Disorders of olfaction and taste are infrequent, but a complete loss of smell or taste reduces the quality of life significantly. The sensitivity of human olfaction is remarkable, even for specific stimuli: Just a few molecules are enough to induce the correct identification of sterilized and ultraheated milk. Olfaction and taste are called 'chemical senses' because in both cases the adequate stimulus consists of molecules that bind to receptors of the sensory cells. The perceptions of smell and taste are often combined. Taste differentiates only four qualities: sweet, sour, salty, and bitter. The typical flavor of food or drink is detected by olfaction. Disturbances of olfaction can be due to respiratory disorders such as nasal polyps, a deviation of the nasal septum or chronic sinusitis. Such conditions can reduce airflow through the olfactory cleft at the roof of the nasal cavity. They can be corrected by modern endoscopic surgery of the nose. Epithelial disorders involving the sensory cells are most often caused by viral infections (influenza-anosmia) or toxic destruction of the sensory epithelium (solvents or gases). Epithelial disorders can be cured only rarely by any treatment. Corticosteroids, zinc, and vitamin A are tried frequently. Neural disorders occur after frontobasal trauma and during neurological diseases such as Parkinson's or Alzheimer's disease. Disorders of olfaction can be an early sign of such neurological diseases and sophisticated examination of this sense can contribute to their early diagnosis. However, no specific treatments have yet been identified. Disorders of taste can be due to toxic, chemical or inflammatory damage to the sensory cells of the tongue.

Essex Neurosciences Centre, Oldchurch Hospital, Romford, UK. ChrisHawkes@msn.com

To assess the value of smell testing we used olfactory evoked potentials (OEP) and an identification test in multiple sclerosis, Parkinson's disease, motor neuron disease and Alzheimer's disease. METHODS: The OEP to H2S (20 ppm) was obtained using an olfactometer designed to stimulate olfactory nerve endings only. Odor recognition was assessed by the University of Pennsylvania Smell Identification Test (UPSIT). In all instances the disease was 'definite' based on standard diagnostic criteria. Controls were derived from 156 healthy people. RESULTS: 1) Multiple Sclerosis: 11/72 patients (15%) were abnormal on UPSIT. For OEP there was significant increase of latency and decrease in amplitude in 6/26 patients (23%). 2) Parkinson's Disease: 126/155 (81%) patients had an abnormal UPSIT score. 12/37 (32%) had prolonged latency with normal amplitude measurement on OEP, but 27 had absent or unclear readings. 4/10 with normal UPSIT displayed abnormality on OEP. 3) Motor Neuron Disease: 9/58 (16%) were abnormal on UPSIT. There was significant delay in 1/10 (10%) patients on OEP. 4) Alzheimer's Disease: UPSIT scores were abnormal in all 8 patients examined. OEP was normal in 4 of these who could be tested. CONCLUSION: Smell dysfunction was found in all 4 conditions but most severely in Parkinson's Disease (over 80%). The UPSIT in general showed abnormality more frequently than OEP. The olfactory defect probably involves peripheral structures in all diseases tested except Alzheimer's. A patient with normal olfaction is unlikely to have idiopathic Parkinson's disease.

Department of Clinical Neurology, Ipswich Hospital, Ipswich, IP4 5PD, United Kingdom. ChrisHawkes@msn.com

In Parkinson's disease and Alzheimer's disease there is profound disorder of olfaction. The extent to which this modality is involved in motor neuron disease (MND) has been studied little. To address this further we assessed olfaction by three methods-a smell identification test ("UPSIT") in 58 patients and 135 controls; olfactory-evoked response (OEP) to H2S in 15 patients, and pathological examination of olfactory bulbs obtained from 8 cadavers. It was found that smell identification compared with the controls was slightly worse overall in the MND group as a whole, but only the bulbar patients scored significantly less on the UPSIT. Patients displayed a subtle defect in cheese odor recognition. OEPs were normal in 9 subjects and delayed in 1 subject. The remaining 5 OEPs were unsuccessful. Histopathological studies of olfactory bulbs showed excess lipofuscin deposition in all 8 cases examined, indicating subclinical neuronal damage. Olfactory neurons with a degree of antioxidant defect may be more susceptible to cellular damage than other neuronal groups because of their direct relationship to environmental agents. Overall we found the degree of olfactory dysfunction in MND to be mild and in contrast with the marked changes described by others. Copyright 1998 Academic Press.

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