Research utilizing magnetic resonance imaging (MRI) has been crucial to the understanding of the neuropathological mechanisms behind and clinical identification of Alzheimer's disease (AD) and mild cognitive impairment (MCI). MRI modalities show patterns of brain damage that discriminate AD from other brain illnesses and brain abnormalities that are associated with risk of conversion to AD from MCI and other behavioural outcomes. This review discusses the application of various MRI techniques to and their clinical usefulness in AD and MCI. MRI modalities covered include structural MRI, diffusion tensor imaging (DTI), arterial spin labelling (ASL), magnetic resonance spectroscopy (MRS), and functional MRI (fMRI). There is much evidence supporting the validity of MRI as a biomarker for these disorders; however, only traditional structural imaging is currently recommended for routine use in clinical settings. Future research is needed to warrant the inclusion for more advanced MRI methodology in forthcoming revisions to diagnostic criteria for AD and MCI.
In this retrospective, pilot, observational longitudinal study, the presence of LM CE was associated with progression of cortical atrophy over 5 years.
Alzheimer's disease (AD) is a devastating and progressive neurodegenerative disease for which there is no cure. Mild cognitive impairment (MCI) is considered a prodromal stage of the disease. Molecular imaging with positron emission tomography (PET) allows for the in vivo visualisation and tracking of pathophysiological changes in AD and MCI. PET is a very promising methodology for differential diagnosis and novel targets of PET imaging might also serve as biomarkers for disease‐modifying therapeutic interventions. This review provides an overview of the current status and applications of in vivo molecular imaging of AD pathology, specifically amyloid, tau, and microglial activation. PET imaging studies were included and evaluated as potential biomarkers and for monitoring disease progression. Although the majority of radiotracers showed the ability to discriminate AD and MCI patients from healthy controls, they had various limitations that prevent the recommendation of a single technique or tracer as an optimal biomarker. Newer research examining amyloid, tau, and microglial PET imaging in combination suggest an alternative approach in studying the disease process.
The presence of RBD in PD is associated with faster motor progression in patients with greater synuclein and dopaminergic pathology, and with higher risk of cognitive decline in patients with greater synuclein and amyloid pathology. Our findings provide an important direction toward understanding phenotypes and their prognosis in PD.
The traditional concept of multiple sclerosis (MS), that it is primarily a white matter inflammatory disease, has changed a great deal. Thanks to the recent development witnessed in MS research, a whole new idea has emerged that MS is a neurodegenerative disease, and neurodegeneration occurs rather earlier in the pathological process. This has also led to the foundation of the hypothesis that two fundamentally different diseases, Alzheimer's disease (AD) and MS, may share a common mechanism of neurodegeneration. Conventionally, amyloid is thought to be a consequence of protein misfolding and aggregation and is most notorious for its association with debilitating and chronic human diseases. Amyloid is implicated to be related with the deterioration and progression of AD. The finding of amyloid precursor protein expression in axons around the plaque in MS, as well as the correlation of amyloid-β (Aβ) with different stages of MS, has clearly indicated that amyloid plays some kind of key role in MS disease pathogenesis. Excitingly, a paradoxical phenomenon of Aβ has also been observed in several studies recently. It has been shown that amyloid might actually be helping in ameliorating the inflammatory effect in diseases like AD and MS. Amyloid imaging allows earlier diagnosis of MS by taking advantage of the relation of amyloid with MS. This will have a big impact on patient diagnosis and management. In this review I have included the findings of research studies dating from several years back to the most recent ones. Through this review I have tried to show the critical role of amyloid in MS and the importance of investigating through PET imaging.
Increased collateral facial vein (FV) flow may be associated with structural damage in patients with multiple sclerosis (MS). The objective was to assess differences in FV flow and magnetic resonance imaging (MRI)-derived outcomes in MS. The study included 136 MS patients who underwent neck and head vascular system examination by echo-color Doppler. Inflammatory MRI markers were assessed on a 3T MRI using a semi-automated edge detection and contouring/thresholding technique. MRI volumetric outcomes of whole brain (WB), gray matter (GM), white matter (WM), cortex, ventricular cerebrospinal fluid (vCSF), deep gray matter (DGM), thalamus, caudate nucleus (CN), putamen, globus pallidus (GP), and hippocampus were calculated. Independent t-test and ANCOVA, adjusted for age, were used to compare groups based on FV flow quartiles. Thirty-four MS patients with FV flow ≤327.8 mL/min (lowest quartile) had significantly lower WB (P<0.001), WM (P<0.001), thalamus (P=0.004), cortex (P=0.004), GM (P=0.004), DGM (P=0.008), hippocampus (P=0.005), and GP volumes (P=0.044) compared to 102 patients with FV flow of >327.8 mL/min (higher quartiles). There were no differences in T1-, T2-and gadolinium-enhancing lesion volumes between the quartile groups.The lack of an association between FV blood flow and inflammatory MRI measures in MS patients, but an association with brain atrophy, suggests that the severity of neurodegenerative process may be related to hemodynamic alterations. MS patients with more advanced global and regional brain atrophy showed low or retrograde FV volume flow.
Background No longitudinal, long-term, follow-up studies have explored the association between presence and severity of variations in extracranial venous anatomy, and clinical outcomes in patients with multiple sclerosis (MS). Objective This prospective 5-year follow-up study assessed the relationship of variations in extracranial venous anatomy, indicative of chronic cerebrospinal venous insufficiency (CCSVI) on Doppler sonography, according to the International Society for Neurovascular Disease (ISNVD) proposed consensus criteria, with clinical outcomes and disease progression in MS patients. Methods 90 MS patients (52 relapsing-remitting, RRMS and 38 secondary-progressive, SPMS) and 38 age- and sex-matched HIs were prospectively followed for 5.5 years. Extracranial and transcranial Doppler-based venous hemodynamic assessment was conducted at baseline and follow-up to determine the extent of variations in extracranial venous anatomy. Change in Expanded Disability Status Scale (∆EDSS), development of disability progression (DP) and annualized relapse rate (ARR) were assessed. Results No significant differences were observed in MS patients, based on their presence of variations in extracranial venous anatomy at baseline or at the follow-up, in ∆EDSS, development of DP or ARR. While more MS patients had ISNVD CCSVI criteria fulfilled at baseline compared to HIs (58% vs. 37%, p = 0.03), no differences were found at the 5-year follow-up (61% vs. 56%, p = 0.486). Discussion This is the longest follow-up study assessing the longitudinal relationship between the presence of variations in extracranial venous anatomy and clinical outcomes in MS patients. Conclusion: The presence of variations in extracranial venous anatomy does not influence clinical outcomes over the 5-year follow-up in MS patients. Electronic supplementary material The online version of this article (10.1186/s12883-019-1350-2) contains supplementary material, which is available to authorized users.
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