Olfactory dysfunction in Alzheimer’s disease Systematic review and meta-analysis

Silva, Maren de Moraes E; Mercer, Pilar Bueno Siqueira; Witt, Maria Carolina Zavagna; Pessoa, Renata Ramina

doi:10.1590/1980-57642018dn12-020004

Cited by 62 publications

(41 citation statements)

References 68 publications

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“…Recent studies have established anosmia as a prodromal biomarker for Alzheimer's disease (48)(49)(50) and the presence of olfactory deficits in a subset of MS patients correlating with symptom severity (51,52). GAS-infected mice show severe persistent physiological deficits in M/ T neuronal function (Fig.…”

Section: Discussionmentioning

confidence: 99%

Th17 lymphocytes drive vascular and neuronal deficits in a mouse model of postinfectious autoimmune encephalitis

Platt

Bolding

Wayne

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Antibodies against neuronal receptors and synaptic proteins are associated with a group of ill-defined central nervous system (CNS) autoimmune diseases termed autoimmune encephalitides (AE), which are characterized by abrupt onset of seizures and/or movement and psychiatric symptoms. Basal ganglia encephalitis (BGE), representing a subset of AE syndromes, is triggered in children by repeated group AStreptococcus(GAS) infections that lead to neuropsychiatric symptoms. We have previously shown that multiple GAS infections of mice induce migration of Th17 lymphocytes from the nose into the brain, causing blood–brain barrier (BBB) breakdown, extravasation of autoantibodies into the CNS, and loss of excitatory synapses within the olfactory bulb (OB). Whether these pathologies induce functional olfactory deficits, and the mechanistic role of Th17 lymphocytes, is unknown. Here, we demonstrate that, whereas loss of excitatory synapses in the OB is transient after multiple GAS infections, functional deficits in odor processing persist. Moreover, mice lacking Th17 lymphocytes have reduced BBB leakage, microglial activation, and antibody infiltration into the CNS, and have their olfactory function partially restored. Th17 lymphocytes are therefore critical for selective CNS entry of autoantibodies, microglial activation, and neural circuit impairment during postinfectious BGE.

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Section: Discussionmentioning

confidence: 99%

Th17 lymphocytes drive vascular and neuronal deficits in a mouse model of postinfectious autoimmune encephalitis

Platt

Bolding

Wayne

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…Nevertheless, a meta-analysis 22 showed that olfactory dysfunction occurs in the initial stages of AD and, thus, may be a preclinical indicator of AD. Several studies 23,24 have also shown olfactory impairment associated with spatial memory loss in AD. AD is characterized by excessive accumulation of toxic forms of amyloid-beta (Aβ).…”

Section: Discussionmentioning

confidence: 99%

“…We believe that the pathology of impaired CSF flow is one of the pathophysiological mechanisms of brain injury in neurodegenerative diseases. It has been described in olfactory dysfunction as well as in patients with idiopathic intracranial hypertension (IIH), AD and glaucoma …”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid and optic nerve sheath compartment syndrome: A common pathophysiological mechanism in five different cases?

Hao

Pircher

Miller

et al. 2019

Clinical Exper Ophthalmology

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Importance Optic nerve (ON) dysfunction is a common feature of different diseases. The pathophysiology is not yet fully understood. Background This study describes five patients with ON sheath (ONS) compartment syndrome (ONSCS) and contributes to the hypothesis that impaired cerebrospinal fluid (CSF) flow can play a role in the development of ON dysfunction. Design Retrospective case series. Participants Five patients with ONSCS were included in the study. Methods Elaboration of medical histories and clinical and diagnostic findings over a long time period was carried out by analysing medical records and by a detailed medical consultation. Main Outcome Measures The main outcome measures include clinical history; visual acuity; field, intraocular and CSF pressures; and contrast‐loaded computed tomographic (CT) cisternography. Results Compartmentation of the ONS demonstrated by contrast‐loaded CT cisternography was the consistent finding in all five patients who demonstrated findings of ON dysfunction. The aetiologies varied and included meningitis, papilloedema, sphenoid wing meningioma, disc herniation and normal‐tension glaucoma. Conclusion and Relevance Compartmentation of the ONS with consecutively impaired CSF dynamics within the ON subarachnoid space can lead to ON dysfunction. Different aetiologies can cause the development of ONSCS.

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“…Due to the culture-specific nature of smell perception, the reliability of these tests has to be evaluated in different populations (2) (37). Localized versions of the UPSIT test kit have been introduced in countries such as Brazil (23), Turkey (24), Lithuania (25), and Iran (16) (for an exhaustive review refer to (14)).…”

Section: Methodsmentioning

confidence: 99%

“…In addition to the mentioned assessment methods, previous studies have shown that olfactory deficit is an early symptom of Alzheimer’s disease (12) (13). Further studies have demonstrated that standard methods of assessing olfactory system such as sniffing kits can be helpful in distinguishing AD patients from healthy individuals (14) (15) (16).…”

Section: Introductionmentioning

confidence: 99%

Olfactory Response as a Marker for Alzheimer's Disease: Evidence from Perceptual and Frontal Oscillation Coherence Deficit

Sedghizadeh

Hojjati

Ezzatdoost

et al. 2019

Preprint

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High-frequency oscillations of the frontal cortex are involved in functions of the brain that fuse processed data from different sensory modules or bind them with elements stored in the memory. These oscillations also provide inhibitory connections to neural circuits that perform lower-level processes. Deficit in the performance of these oscillations has been examined as a marker for Alzheimer's disease (AD). Additionally, the neurodegenerative processes associated with AD, such as the deposition of amyloid-beta plaques, do not occur in a spatially homogeneous fashion and progress more prominently in the medial temporal lobe in the early stages of the disease. This region of the brain contains neural circuitry involved in olfactory perception. Several studies have suggested that olfactory deficit can be used as a marker for early diagnosis of AD. A quantitative assessment of the performance of the olfactory system can hence serve as a potential biomarker for Alzheimer's disease, offering a relatively convenient and inexpensive diagnosis method. This study examines the decline in the perception of olfactory stimuli and the deficit in the performance of high-frequency frontal oscillations in response to olfactory stimulation as markers for AD. Two measurement modalities are employed for assessing the olfactory performance: 1) An interactive smell identification test is used to sample the response to a sizable variety of odorants, and 2) Electrophysiological data are collected in an olfactory perception task with a pair of selected odorants in order to assess the connectivity of frontal cortex regions. Statistical analysis methods are used to assess the significance of selected features extracted from the recorded modalities as Alzheimer's biomarkers. Olfactory decline regressed to age in both healthy and Mild AD groups are evaluated, and single- and multi-modal classifiers are also developed. The novel aspects of this study include: 1) Combining EEG response to olfactory stimulation with behavioral assessment of olfactory perception as a marker of AD, 2) Identification of odorants most significantly affected in Mild AD patients, 3) Identification of odorants which are still adequately perceived by Mild AD patients, 4) Analysis of the decline in the spatial coherence of different oscillatory bands in response to olfactory stimulation, and 5) Being the first study to quantitatively assess the performance of olfactory decline due to aging and AD in the Iranian population.

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Olfactory dysfunction in Alzheimer’s disease Systematic review and meta-analysis

Cited by 62 publications

References 68 publications

Th17 lymphocytes drive vascular and neuronal deficits in a mouse model of postinfectious autoimmune encephalitis

Th17 lymphocytes drive vascular and neuronal deficits in a mouse model of postinfectious autoimmune encephalitis

Cerebrospinal fluid and optic nerve sheath compartment syndrome: A common pathophysiological mechanism in five different cases?

Olfactory Response as a Marker for Alzheimer's Disease: Evidence from Perceptual and Frontal Oscillation Coherence Deficit

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