Olfactory Identification and Incidence of Mild Cognitive Impairment in Older Age

Wilson, Robert S.; Schneider, Julie A.; Arnold, Steven E.; Tang, Yuxiao; Boyle, Patricia A.; Bennett, David A.

doi:10.1001/archpsyc.64.7.802

Cited by 255 publications

(238 citation statements)

References 64 publications

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“…[3][4][5] Thus, it is not surprising that olfactory tests have been considered as simple tools for early diagnosis of various neuropsychiatric disorders. 3,4,6 Early and specific diagnosis is of vital importance for successful treatment of neurodegenerative disorders, including Alzheimer-type dementia, in older adults. A growing body of evidence indicates that patients with Alzheimer-type dementia suffer from marked olfactory dysfunction, including deficits in olfactory acuity (e.g.…”

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confidence: 99%

“…In line with the above, it has been reported that olfactory tests facilitate screening for dementia in the elderly. 3,6 It is widely recognized that depressive symptoms can mimic cognitive impairment and dementia in older patients. 7 Therefore, it has been suggested that olfactory tests could also improve differential diagnosis between dementia and depression in older subjects.…”

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confidence: 99%

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Depressive symptoms and olfactory function in older adults

Ścińska

Wróbel

Korkosz

et al. 2008

Psychiatry Clin Neurosci

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Aims: Neuroimaging studies suggest a significant overlap between brain regions involved in the regulation of olfaction and mood. The aim of the present study was to search for correlations between depressive symptomatology measured by the 15-item Geriatric Depression Scale (GDS) and olfactory function assessed with Sniffin' Sticks in non-demented older adults (aged 53-79 years).Methods: Taste detection thresholds were also measured by means of electrogustometry on the anterior tongue. Results:No correlation was found between the GDS scores (range: 0-12) and olfactory thresholds or olfactory identification scores. Similarly, there was no relationship between depressive symptoms and electrogustometric thresholds. Subjects (n = 25) scoring Ն5 on the GDS were classified as 'depressed' and all other individuals (n = 60) were classified as 'nondepressed'. The two groups did not differ in terms of the olfactory measures and electrogustometric threshold. Conclusion:Depressive symptoms are not associated with any major olfactory deficit in non-clinical older adults.

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confidence: 99%

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confidence: 99%

Depressive symptoms and olfactory function in older adults

Ścińska

Wróbel

Korkosz

et al. 2008

Psychiatry Clin Neurosci

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“…The hippocampus plays a critical role in the acquisition and retrieval of declarative memory (52), which is prominently impaired in AD subjects (53,54). Olfactory dysfunction is also an incipient symptom of AD (55,56). When considered together with our previous data, we can show that Ab load is associated with increases in caspase-4 (1) in vitro, (2) in the AD mouse model, and (3) in AD patients (25).…”

Section: Discussionmentioning

confidence: 68%

The human-specificCASP4gene product contributes to Alzheimer-related synaptic and behavioural deficits

Kajiwara¹,

McKenzie

Dorr

et al. 2016

Hum. Mol. Genet.

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Recent studies have indicated that innate immune signalling molecules are involved in late-onset Alzheimer's disease (LOAD) risk. Amyloid beta (Ab) accumulates in AD brain, and has been proposed to act as a trigger of innate immune responses. Caspase-4 is an important part of the innate immune response. We recently characterized transgenic mice carrying human CASP4, and observed that the mice manifested profound innate immune responses to lipopolysaccharide (LPS). Since these inflammatory processes are important in the aetiology of AD, we have now analysed the correlation of expression of caspase-4 in human brain with AD risk genes, and studied caspase-4 effects on AD-related phenotypes in APPswe/PS1deltaE9 (APP/PS1) mice. We observed that the expression of caspase-4 was strongly correlated with AD risk genes including TYROBP, TREM2, CR1, PSEN1, MS4A4A and MS4A6A in LOAD brains. Caspase-4 expression was upregulated in CASP4/APP/PS1 mice in a region-specific manner, including hippocampus and prefrontal cortex. In APP/PS1 mice, caspase-4 expression led to impairments in the reversal phase of a Barnes maze task and in hippocampal synaptic plasticity, without affecting soluble or aggregated Ab levels. Caspase-4 was expressed predominantly in microglial cells, and in the presence of CASP4, more microglia were clustered around amyloid plaques. Furthermore, our data indicated that caspase-4 modulates microglial cells in a manner that increases proinflammatory processes. We propose that microglial caspase-4 expression contributes to the cognitive impairments in AD, and that further study of caspase-4 will enhance our understanding of AD pathogenesis and may lead to novel therapeutic targets in AD.

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“…The autopsy outcomes suggested that in elderly the olfactory identification deficit is partly due to the accumulation of NFT in the primary olfactory cortex. Hyposmia can predict the next start of mild cognitive impairment (MCI) in patients with a not yet measurable cognitive impairment (Wilson et al, 2007b) and an increased risk of AD was demonstrated in MCI patients with hyposmia associated with unawareness of the olfactory deficit (Devanand et al, 2000). Conversely Bahar-Fucks et al suggest that unawareness of olfactory deficit does not improve the identification of patients with MCI progressing to AD (Bahar-Fuchs et al, 2011).…”

Section: The Role Of Olfactory Test In Alzheimer's Diseasementioning

confidence: 99%