Limits...
Cerebral amyloid angiopathy: emerging concepts.

Yamada M - J Stroke (2015)

Bottom Line: Cerebrovascular Aβ deposits accompany functional and pathological changes in cerebral blood vessels (CAA-associated vasculopathies).Moreover, cSS is closely associated with transient focal neurological episodes (TFNE).This article reviews CAA and CAA-related disorders with respect to their epidemiology, pathology, pathophysiology, clinical features, biomarkers, diagnosis, treatment, risk factors, and future perspectives.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.

ABSTRACT
Cerebral amyloid angiopathy (CAA) involves cerebrovascular amyloid deposition and is classified into several types according to the amyloid protein involved. Of these, sporadic amyloid β-protein (Aβ)-type CAA is most commonly found in older individuals and in patients with Alzheimer's disease (AD). Cerebrovascular Aβ deposits accompany functional and pathological changes in cerebral blood vessels (CAA-associated vasculopathies). CAA-associated vasculopathies lead to development of hemorrhagic lesions [lobar intracerebral macrohemorrhage, cortical microhemorrhage, and cortical superficial siderosis (cSS)/focal convexity subarachnoid hemorrhage (SAH)], ischemic lesions (cortical infarction and ischemic changes of the white matter), and encephalopathies that include subacute leukoencephalopathy caused by CAA-associated inflammation/angiitis. Thus, CAA is related to dementia, stroke, and encephalopathies. Recent advances in diagnostic procedures, particularly neuroimaging, have enabled us to establish a clinical diagnosis of CAA without brain biopsies. Sensitive magnetic resonance imaging (MRI) methods, such as gradient-echo T2(*) imaging and susceptibility-weighted imaging, are useful for detecting cortical microhemorrhages and cSS. Amyloid imaging with amyloid-binding positron emission tomography (PET) ligands, such as Pittsburgh Compound B, can detect CAA, although they cannot discriminate vascular from parenchymal amyloid deposits. In addition, cerebrospinal fluid markers may be useful, including levels of Aβ40 for CAA and anti-Aβ antibody for CAA-related inflammation. Moreover, cSS is closely associated with transient focal neurological episodes (TFNE). CAA-related inflammation/angiitis shares pathophysiology with amyloid-related imaging abnormalities (ARIA) induced by Aβ immunotherapies in AD patients. This article reviews CAA and CAA-related disorders with respect to their epidemiology, pathology, pathophysiology, clinical features, biomarkers, diagnosis, treatment, risk factors, and future perspectives.

No MeSH data available.


Related in: MedlinePlus

Amyloid positron emission tomography (PET) using 11C-Pittsburgh Compound B (PiB) (A) with gradient echo T2*-weighted MRI (B) in a non-demented patient with multiple CAA-related intracerebral hemorrhages and disseminated cortical superficial siderosis. The left parietal region with an old intracerebral hemorrhage shows a relative scarcity of PiB uptake.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4325636&req=5

Figure 5: Amyloid positron emission tomography (PET) using 11C-Pittsburgh Compound B (PiB) (A) with gradient echo T2*-weighted MRI (B) in a non-demented patient with multiple CAA-related intracerebral hemorrhages and disseminated cortical superficial siderosis. The left parietal region with an old intracerebral hemorrhage shows a relative scarcity of PiB uptake.

Mentions: Amyloid imaging with the PET ligand, PiB, revealed an increase of PiB binding that often shows greater occipital uptake in CAA-related ICH (Figure 5).75,76,77 Microhemorrhages are associated with PiB retention,33,34 and new CAA-related hemorrhages preferentially occur at sites of PiB retention.35 As a frequent occurrence of high PiB uptake in healthy elderly individuals reflects incipient AD, PiB PET has low specificity for CAA; however, a negative PiB scan rules out CAA with excellent sensitivity.78 Amyloid imaging with such PET ligands as PiB cannot discriminate vascular from parenchymal deposition or Aβ from other amyloid proteins; reagents specific for vascular Aβ deposition are favorable candidates for amyloid imaging specific for Aβ-type CAA.79


Cerebral amyloid angiopathy: emerging concepts.

Yamada M - J Stroke (2015)

Amyloid positron emission tomography (PET) using 11C-Pittsburgh Compound B (PiB) (A) with gradient echo T2*-weighted MRI (B) in a non-demented patient with multiple CAA-related intracerebral hemorrhages and disseminated cortical superficial siderosis. The left parietal region with an old intracerebral hemorrhage shows a relative scarcity of PiB uptake.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4325636&req=5

Figure 5: Amyloid positron emission tomography (PET) using 11C-Pittsburgh Compound B (PiB) (A) with gradient echo T2*-weighted MRI (B) in a non-demented patient with multiple CAA-related intracerebral hemorrhages and disseminated cortical superficial siderosis. The left parietal region with an old intracerebral hemorrhage shows a relative scarcity of PiB uptake.
Mentions: Amyloid imaging with the PET ligand, PiB, revealed an increase of PiB binding that often shows greater occipital uptake in CAA-related ICH (Figure 5).75,76,77 Microhemorrhages are associated with PiB retention,33,34 and new CAA-related hemorrhages preferentially occur at sites of PiB retention.35 As a frequent occurrence of high PiB uptake in healthy elderly individuals reflects incipient AD, PiB PET has low specificity for CAA; however, a negative PiB scan rules out CAA with excellent sensitivity.78 Amyloid imaging with such PET ligands as PiB cannot discriminate vascular from parenchymal deposition or Aβ from other amyloid proteins; reagents specific for vascular Aβ deposition are favorable candidates for amyloid imaging specific for Aβ-type CAA.79

Bottom Line: Cerebrovascular Aβ deposits accompany functional and pathological changes in cerebral blood vessels (CAA-associated vasculopathies).Moreover, cSS is closely associated with transient focal neurological episodes (TFNE).This article reviews CAA and CAA-related disorders with respect to their epidemiology, pathology, pathophysiology, clinical features, biomarkers, diagnosis, treatment, risk factors, and future perspectives.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.

ABSTRACT
Cerebral amyloid angiopathy (CAA) involves cerebrovascular amyloid deposition and is classified into several types according to the amyloid protein involved. Of these, sporadic amyloid β-protein (Aβ)-type CAA is most commonly found in older individuals and in patients with Alzheimer's disease (AD). Cerebrovascular Aβ deposits accompany functional and pathological changes in cerebral blood vessels (CAA-associated vasculopathies). CAA-associated vasculopathies lead to development of hemorrhagic lesions [lobar intracerebral macrohemorrhage, cortical microhemorrhage, and cortical superficial siderosis (cSS)/focal convexity subarachnoid hemorrhage (SAH)], ischemic lesions (cortical infarction and ischemic changes of the white matter), and encephalopathies that include subacute leukoencephalopathy caused by CAA-associated inflammation/angiitis. Thus, CAA is related to dementia, stroke, and encephalopathies. Recent advances in diagnostic procedures, particularly neuroimaging, have enabled us to establish a clinical diagnosis of CAA without brain biopsies. Sensitive magnetic resonance imaging (MRI) methods, such as gradient-echo T2(*) imaging and susceptibility-weighted imaging, are useful for detecting cortical microhemorrhages and cSS. Amyloid imaging with amyloid-binding positron emission tomography (PET) ligands, such as Pittsburgh Compound B, can detect CAA, although they cannot discriminate vascular from parenchymal amyloid deposits. In addition, cerebrospinal fluid markers may be useful, including levels of Aβ40 for CAA and anti-Aβ antibody for CAA-related inflammation. Moreover, cSS is closely associated with transient focal neurological episodes (TFNE). CAA-related inflammation/angiitis shares pathophysiology with amyloid-related imaging abnormalities (ARIA) induced by Aβ immunotherapies in AD patients. This article reviews CAA and CAA-related disorders with respect to their epidemiology, pathology, pathophysiology, clinical features, biomarkers, diagnosis, treatment, risk factors, and future perspectives.

No MeSH data available.


Related in: MedlinePlus