Reduced olfactory bulb and tract volume in early Alzheimer's disease—A MRI study

Thomann, Philipp A.; Santos, Vasco Dos; Toro, Pablo; Schönknecht, Peter; Essig, Marco; Schröder, Johannes

doi:10.1016/j.neurobiolaging.2007.08.001

Cited by 125 publications

(78 citation statements)

References 14 publications

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“…Thus, altered cholesterol homeotasis could contribute to the development of olfactory dysfunction in sporadic AD. Pathologically, oxidative damage, the presence of Aβ plaque, and accumulation of phosphorylated tau as neurofilrillary tangles all have been documented in olfactory epithelium and olfactory bulbs of AD patients [44][45][46][47][48][49][50][51]. Previously we showed in olfactory bulb from cholesterol-fed rabbits that elevated levels of circulating cholesterol disrupted the blood-brain barrier [16], increased accumulations of cholesterol in endolysosomes of neurons in olfactory bulb originated from peripheral sources, and contributed to the development of AD-like pathology including synaptic loss, elevated Aβ production, and increased tau phosphorylation [7].…”

Section: Discussionmentioning

confidence: 99%

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

Chen¹,

Tian²,

Ghribi³

et al. 2016

J Integr Syst Neurosci

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The pathogenesis of sporadic AD is believed to result from complex interactions between nutritional, environmental, epigenetic and genetic factors. Among those factors, elevated plasma cholesterol, independent of APOE genotypes, is strongly linked to the pathogenesis of sporadic AD, whereas chronic ingestion of caffeine is protective against sporadic AD. Others and we have shown that rabbits-fed cholesterol-enriched diet exhibit early AD-like pathological features including bloodbrain barrier (BBB) leakage and endolysosome dysfunction, as well as, AD-like pathological hallmarks including synaptic disruption, increased intraneuronal and brain deposition of amyloid beta (Aβ), and tau pathology. Further, we found that caffeine protects against the cholesterol-induced increases in BBB permeability. Here, we determined the extent to which caffeine affects cholesterol-enriched diet-induced increases in other pathological features of AD. We demonstrated that caffeine administration at low and moderate doses did not affect plasma levels of cholesterol, but did block significantly cholesterol-enriched diet-induced increases in brain levels of apoB and accumulation of apoB in neuronal endolysosomes. Furthermore, we demonstrated that caffeine administration at the two doses blocked cholesterol-enriched diet-induced abnormal accumulation of synaptophysin, Aβ, and phosphorylated tau in endolysosomes. Our findings suggest that caffeine exerts its protective effects against the development of sporadic AD-like pathological features, in part, by preventing the entrance of LDL cholesterol into brain parenchyma, the accumulation of LDL-cholesterol in neuronal endolysosomes, and structural and functional changes to endolysosomes.

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Section: Discussionmentioning

confidence: 99%

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

Chen¹,

Tian²,

Ghribi³

et al. 2016

J Integr Syst Neurosci

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show abstract

“…The scoring system used in this study is a simple 4-point system: 1 point for all numbers (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12) present and in the correct sequence; 1 point for correct spatial orientation and placement Boston Naming Test -BNT [24] is a 60-item test used to assess visual naming ability using black and white drawings of common objects.…”

Section: Methodsmentioning

confidence: 99%

“…Wilson et al [9] found that the density of tangles present in the central olfactory system, the entorhinal cortex and CA1/subiculum region of the hippocampus, was inversely related to odor identification ability. It is not suprising that olfactory deficit are apparent even in the earliest stages of AD given that the earliest pathologic changes in AD appear to take place within the transentorhinal and entorhinal cortex [2,5,7,10,11]. This area of the brain is important both for memory consolidation and the processing of olfactory information [2].…”

Section: Several Different Odor Identification Testsmentioning

confidence: 99%

Odor identification and cognitive abilities in Alzheimer’s disease

Tkalčić

Spasic

Ivanković

et al. 2011

Translational Neuroscience

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Research results indicate systemic odor identification deficits in patients with Alzheimer's disease (AD). The aims of this study were: 1) to compare the ability to identify different odors and to compare cognitive status among patients with AD, patients with vascular dementia (VaD) and a comparison group of elderly persons; 2) to test the efficiency of olfactory and neuropsychological measures to classify patients and 3) to relate the odor identification ability with cognitive functioning for each group, respectively. The participants were 15 patients with AD, 11 patients with VaD and 30 non-demented elderly persons, age range 58 to 90. To assess olfactory function, we used the Scandinavian Odor-Identification Test. To assess cognitive functions, we used the Dementia Rating Scale-2, the Clock Drawing Test, the Boston Naming Test and the Category Fluency Test. The ANOVA showed that patients with AD correctly identifed significantly fewer odors presented to them compared to patients with VaD and control group. Patients with AD achieved significantly lower scores on all neuropsychological measures compared to the control group and differ in the DRS-2 total score, initiation/ perseveration, constructive and naming abilities comparing to patients with VaD. Discriminant analysis showed that category fluency and olfactory identification were the best predictors of AD. Significant correlations were found between the olfactory and initiation/perseveration, memory and animal naming abilities for patients with AD. Differences among patients with AD, VaD and elderly persons exist in their abilities to identify odors. The findings suggest that olfactory functional testing in combination with memory testing are important.

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“…The degree of atrophy correlated with the global cognitive performance as measured by the Mini Mental State Examination scores [54].…”

Section: Translational Neurosciencementioning

confidence: 96%

“…Using magnetic resonance (MR) volumetric measurements, Thomann et al [53,54] found that, compared to age-matched controls, the most severe atrophy of the OB and OT was seen in AD; but, atrophy was already found in mild cognitive impairment (MCI), suggesting early involvement of the olfactory system. The degree of atrophy correlated with the global cognitive performance as measured by the Mini Mental State Examination scores [54].…”

Section: Translational Neurosciencementioning

confidence: 99%

The olfactory system in Alzheimer’s disease: Pathology, pathophysiology and pathway for therapy

Kovács

2013

Translational Neuroscience

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Olfaction is frequently mentioned as a "neglected sense", although the olfactory system has several interesting and unique anatomical and physiological features. Olfactory involvement is present in several degenerative disorders, especially in Alzheimer's disease (AD). The peripheral and central parts of the olfactory system are damaged even in the early stages of AD, manifesting in profound olfactory deficits. Besides the early pathology, the olfactory system may be involved in the pathogenesis of AD by providing a route of entry for pathological agents still unknown. In contrast to this olfactory vector hypothesis, the olfactory system can be used to deliver therapeutic agents in AD, such as nerve growth factor and insulin, by decreasing the side-effects of the therapy or providing a non-invasive method of delivery.

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Reduced olfactory bulb and tract volume in early Alzheimer's disease—A MRI study

Cited by 125 publications

References 14 publications

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

Odor identification and cognitive abilities in Alzheimer’s disease

The olfactory system in Alzheimer’s disease: Pathology, pathophysiology and pathway for therapy

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