Abstract:A 77 year-old men developed a subacute-onset, rapidly progressive cognitive
decline. After 6 months of evolution, he scored 6 on the Mini-Mental State
Examination and had left hemiparesis and hemineglect. The patient died 11 months
after the onset of cognitive symptoms. Brain MRI showed microhemorrhages on
gradient-echo sequence and confluent areas of white matter hyperintensities on
T2-weighted images. Brain biopsy revealed amyloid-β peptide deposition in
vessel walls, some of them surrounded by micro-bleeds.… Show more
“…Furthermore, hypometabolism based on Fluoro‐2‐deoxyglucose ([ 18 F]‐FDG) PET, which is considered a marker of neuronal dysfunction, has been shown to be a prominent feature in early AD, particularly in the posterior parietal and cingulate regions . Although the extracellular amyloid deposition is not directly correlated with detectable vascular injury (i.e., cerebral amyloid angiopathy, CAA) , its association with white matter damage and RS‐fMRI changes in different stages of dementia needs to be further examined .…”
Purpose
To quantify and investigate the interactions between multimodal MRI/positron emission tomography (PET) imaging metrics in elderly patients with early Alzheimer's disease (AD), mild cognitive impairment (MCI) and healthy controls.
Materials and Methods
Thirteen early AD, 17 MCI patients, and 14 age-matched healthy aging controls from the Alzheimer's Disease Neuroimaging Initiative database were selected based on availability of data. Default mode network (DMN) functional connectivity and fractional amplitude of low frequency fluctuation (fALFF) were obtained for resting state functional MRI (RS-fMRI). White matter lesion load (WMLL) was quantified from MRI T2-weighted FLAIR images. Amyloid deposition with PET [18F]-Florbetapir tracer and metabolism of glucose by means of [18F]-fluoro-2-deoxyglucose (FDG) images were quantified using ratio of standard uptake values (rSUV).
Results
Whole-brain WMLL and amyloid deposition were significantly higher (P < 0.005) in MCI and AD patients compared with controls. RS-fMRI results showed significantly reduced (corrected P < 0.05) DMN connectiv ity and altered fALFF activity in both MCI and AD groups. FDG uptake results showed hypometabolism in AD and MCI patients compared with controls. Correlations (P < 0.05) were found between WMLL and amyloid load, FDG uptake and amyloid load, as well as between amyloid load (rSUV) and fALFF.
Conclusion
Our quantitative results of four MRI and PET imaging metrics (fALFF/DMN, WMLL, amyloid, and FDG rSUV values) agree with published values. Signifi-cant correlations between MRI metrics, including WMLL/ functional activity and PET amyloid load suggest the potential of MRI and PET-based biomarkers for early detection of AD.
“…Furthermore, hypometabolism based on Fluoro‐2‐deoxyglucose ([ 18 F]‐FDG) PET, which is considered a marker of neuronal dysfunction, has been shown to be a prominent feature in early AD, particularly in the posterior parietal and cingulate regions . Although the extracellular amyloid deposition is not directly correlated with detectable vascular injury (i.e., cerebral amyloid angiopathy, CAA) , its association with white matter damage and RS‐fMRI changes in different stages of dementia needs to be further examined .…”
Purpose
To quantify and investigate the interactions between multimodal MRI/positron emission tomography (PET) imaging metrics in elderly patients with early Alzheimer's disease (AD), mild cognitive impairment (MCI) and healthy controls.
Materials and Methods
Thirteen early AD, 17 MCI patients, and 14 age-matched healthy aging controls from the Alzheimer's Disease Neuroimaging Initiative database were selected based on availability of data. Default mode network (DMN) functional connectivity and fractional amplitude of low frequency fluctuation (fALFF) were obtained for resting state functional MRI (RS-fMRI). White matter lesion load (WMLL) was quantified from MRI T2-weighted FLAIR images. Amyloid deposition with PET [18F]-Florbetapir tracer and metabolism of glucose by means of [18F]-fluoro-2-deoxyglucose (FDG) images were quantified using ratio of standard uptake values (rSUV).
Results
Whole-brain WMLL and amyloid deposition were significantly higher (P < 0.005) in MCI and AD patients compared with controls. RS-fMRI results showed significantly reduced (corrected P < 0.05) DMN connectiv ity and altered fALFF activity in both MCI and AD groups. FDG uptake results showed hypometabolism in AD and MCI patients compared with controls. Correlations (P < 0.05) were found between WMLL and amyloid load, FDG uptake and amyloid load, as well as between amyloid load (rSUV) and fALFF.
Conclusion
Our quantitative results of four MRI and PET imaging metrics (fALFF/DMN, WMLL, amyloid, and FDG rSUV values) agree with published values. Signifi-cant correlations between MRI metrics, including WMLL/ functional activity and PET amyloid load suggest the potential of MRI and PET-based biomarkers for early detection of AD.
“…Indeed, there are few similar cases in the literature available. In the clinical case described by Takada et al [18], the patient had a rapidly progressive dementia that, after the investigations, they diagnosed as CAA causing RPD. As in our case, they found a slightly increased level of CSF protein, whilst every other parameter in cerebrospinal fluid was normal.…”
The most frequent manifestation of Cerebral Amyloid Angiopathy (CAA) is symptomatic, spontaneous Intracerebral Hemorrhage (ICH), preferentially affecting lobar regions. It is the second most common cause of ICH after hypertensive angiopathy in the general population. Other common manifestations are ischemic episodes, transient focal neurological episodes, subarachnoid hemorrhage and cognitive decline. Here, we describe an interesting case of a patient with a clinical picture of a rapidly progressive dementia caused by CAA, to highlight the heterogeneous clinical variability of this condition. The diagnosis and, in particular, the management and therapy of patients affected by CAA or any inflammatory form is often challenging. Our case report shows that CAA without inflammation should be included among the possible cause of rapidly progressive dementia.
“…Realizamos una revisión en las principales bases de datos (Pubmed, Embase, Lilacs y Scielo) y sólo encontramos cinco casos reportados en Latinoamérica con AAC o AAC-IR, uno en México 12 , uno en Uruguay 13 y dos en Brasil 14,15 no relacionados con inflamación y el quinto caso en Argentina asociado a inflamación 16 . En Colombia no encontramos ningún caso reportado de AAC con o sin inflamación.…”
La angiopatía amiloide cerebral (AAC) consiste en el depósito de amiloide en la pared de los vasos sanguíneos intracraneales, y conlleva a la aparición de hemorragia, isquemia o leucoencefalopatía. Las manifestaciones clínicas de la AAC son muy variables, tales como alteraciones cognitivas, alteraciones comportamentales, déficit neurológico focal, cefalea o crisis epilépticas. Un subtipo de angiopatía amiloide cerebral con inflamación relacionada (AAC-IR), se ha reportado recientemente en la literatura mundial. Presentamos el caso de una paciente de 74 años de edad, con un cuadro de demencia rápidamente progresiva de aproximadamente tres meses de evolución, asociada a cefalea, meningismo, disminución de la fuerza en hemicuerpo derecho, múltiples lesiones hemorrágicas parenquimatosas, hemosiderosis difusa, edema cerebral focal y estudio histológico con evidencia de amiloide intracerebral.
El diagnóstico de la AAC se basa en una historia clínica compatible; neuroimagenes que demuestren hemosiderosis o múltiples hemorragias de predominio en fosa posterior, y en algunos casos estudio histológico que confirme la presencia de amiloide en la microcirculación intracraneal. Los criterios de Boston modificados unifican los hallazgos para el diagnóstico de AAC con diferentes grados de certeza. En algunas ocasiones, como en el caso presentado, la AAC se asocia a un componente inflamatorio, y se manifiesta con una demencia rápidamente progresiva, constituyéndose en un verdadero reto diagnóstico.
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