Cerebral amyloidal angiopathy—A disease with implications for neurology and psychiatry

doi:10.1016/j.brainres.2013.04.052

Brain Research

Volume 1519, 26 June 2013, Pages 19-30

https://doi.org/10.1016/j.brainres.2013.04.052 Get rights and content

Abstract

Cerebral Amyloidal Angiopathy (CAA), which occurs sporadically in most cases but can also occur hereditarily, belongs to the group amyloidoses and is characterized by the deposition and accumulation of beta-amyloid (Aβ) in smaller arterial vessels of the brain. The deposition of Aβ leads to degenerative changes in the cerebral vessel system (thickening of the vessel wall, microaneurysm, constriction of vascular lumen, dissection), which favour the development of the clinical symptomatology most often associated with CAA. Besides haemorrhages, cerebral ischaemia, transient neurological symptoms, leukoencephalopathy as well as cognitive decline and even dementia may appear in connection with CAA. A definite diagnosis of CAA can only be made on the basis of a pathological assessment, even though diagnostic findings of cerebral neuroimaging and clinical symptoms allow the diagnosis of a probable CAA. At present, no causal therapy options are available. Although CAA is placed within the range of neurological illnesses, psychiatric symptoms such as cognitive impairment, personality change or behavioural problems as well as depression are plausible clinical manifestations of CAA and may even dominate the clinical picture. Apart from epidemiological, pathogenetical, clinical and diagnostical aspects, possible psychiatric implications of CAA are discussed in the review article.

Introduction

Cerebral Amyloidal Angiopathy (CAA) belongs to the group of amyloidoses (Biffi and Greenberg, 2011), which constitute a heterogenic range of diseases. Amyloidoses are characterized by an interstitial deposition and accumulation of proteins potentially affecting all body tissues, which are modified pathologically as to their secondary structure and are, in most cases, indissoluble (Merlini and Bellotti, 2003). These proteins, existing in the form of fibrillates, are referred to as amyloid and lead to tissue destruction and a progredient impairment of the corresponding organ function (Merlini and Bellotti, 2003, Perfetto et al., 2010). The term Cerebral Amyloidal Angiopathy also refers to a heterogenic group of illnesses of the central nervous system differing by their genetic and biochemical characteristics (Biffi and Greenberg, 2011), which can be characterized histopathologically by the presence of amyloidal fibrils in small to medium-sized, in most cases, arterial vessels of the brain. Spontaneously appearing intracerebral bleeding (ICB), which affects mostly superficial regions of the cortex, constitutes the leading symptom of CAA (Pezzini et al., 2009, Viswanathan and Greenberg, 2011). While the incidence of ICB with patients younger than 75 has decreased these last few years due to efficient antihypertensive pharmacotherapy, patients older than 74 present an increase of said incidence. Besides other factors, this can be explained by the age-dependent incidence of CAA (Lovelock et al., 2007). Clues of CAA can be found with over 50% of patients aged between 70 and 89, while it is rare under the age of 55 (Yoshimura, 2000). On the background of demographic modifications, a further increase in the prevalence of CAA may be observed in the future (Block, 2011).

CAA is considered to be a neurological disease, but can also appear with symptoms requiring psychiatric treatment. The present review paper shall enable an insight into the historical, epidemiologic, pathogenetical and clinical aspects of CAA. Possible psychiatric implications will be discussed as well.

Section snippets

Methods

A narrative review was conducted. In September 2012 the Medline database was searched using the search term “cerebral amyloid angiopathy”. Initally, n=1812 hits were retrieved. Considering only publications written in English the original number of hits decreased to n=1628. Titles and abstracts of these articles were checked for their relevance to this article. Finally, n=147 publications were considered for this review article.

Psychiatric implications of CAA

Though CAA is mainly a neurological illness, it can also appear bearing psychiatric symptoms. Currently there are no studies that address the possible psychiatric implications of CAA systematically. In the following we aim at discussing aspects of CAA that might be relevant to psychiatry.

Due to CAA being a chronic progredient illness of the central nervous system, the development of slight psychiatric symptoms during the disease progression is conceivable, especially in the first stages of CAA,

Conclusions

Apart from the typical clinical presentation of CAA that includes ICB, cerebral ischaemia and transient neurological symptoms such as cognitive impairment and dementia as well as depression, behavioural problems and/or personality change are plausible clinical manifestations of CAA. This implicates that CAA might be a disease with relevance to psychiatry. In this connection it is important to keep in mind that CAA might be the cause for occasionally unspecific psychopathological abnormalities,

Acknowledgments

None.

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Main features of hereditary cerebral amyloid angiopathies: A systematic review
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Citation Excerpt :
Mirroring previous observations in sporadic CAA, individuals diagnosed with hereditary CAA appear to develop progressive cognitive decline owing in large part to two (often coexisting) mechanism: 1) step-wise accumulation of CNS injury due to repeated symptomatic hemorrhagic and/or ischemic strokes; and 2) chronically progressive and diffuse CNS injury due to accumulation of microvascular ischemic and hemorrhagic lesions [34,35] Future studies of CAA-related neurocognitive symptoms will therefore continue to benefit from addressing this mechanistic heterogeneity, which is likely to result in different therapeutic approaches in clinical practice, i.e. acute interventions to limit ICH-related injury vs. long-term treatments to delay or arrest progression of diffuse vasculopathy related to amyloidosis. Recent evidence has also linked CAA to neurobehavioral and neuropsychiatric symptoms as well, chiefly depression and apathy [36–39] However, systematic exploration of these manifestations in hereditary CAA has been limited to date [5] Some forms of familial CAA (those with the Iowa and Arctic mutations in particular) appear to be more consistently associated with neurobehavioral and neuropsychiatric symptoms, usually in the form of personality changes, paranoia, and hallucinations. Minor neuropsychiatric symptoms are occasionally diagnosed among individuals affected by other forms of hereditary CAA, usually in the form of anxiety or depression.
The term Cerebral Amyloid Angiopathy (CAA) refers to a group of neurovascular disorders characterized by amyloid deposition within the walls of leptomeningeal and cortical blood vessels of the brain, with specific predilection for arterioles, and (less often) capillaries and veins. Most CAA cases in the general population are sporadic in nature, and represent primarily an age-related condition affecting individuals in the fifth decade of life and beyond. Sporadic CAA is caused by deposition of amyloid-β (Aβ), originating from proteolytic cleavage of the Amyloid Precursor Protein (APP), within the walls of cerebral small caliber vessels. However, hereditary forms of CAA have also been described, generally presenting as rare familial disorder with monogenic (predominantly autosomal dominant) inheritance patterns. Hereditary CAA forms tend to affect younger individuals, and their course and clinical progression is more severe. Studies to date primarily focused on the vascular manifestations of sporadic and hereditary CAA, chiefly symptomatic lobar Intracerebral Hemorrhage (ICH). However, in the past decade sporadic CAA has also been consistently linked to progressive neurocognitive, neurobehavioral, and neuropsychiatric symptoms. This systematic review focuses on the genetics, pathogenesis, neuroimaging, neuropathology, and clinical manifestations of hereditary CAA with specific emphasis on previously overlooked cognitive, behavioral, and psychiatric symptoms.
Impaired dynamic cerebral autoregulation in patients with cerebral amyloid angiopathy
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Cerebral amyloid angiopathy (CAA) might disturb the sensitive mechanism of cerebral pressure autoregulation. This study examines whether dynamic cerebral autoregulation (CA) is impaired in the posterior or anterior circulation of CAA patients. Fifteen patients with known CAA on magnetic resonance imaging (MRI) and 14 age-matched controls were examined with transcranial Doppler. Dynamic CA was assessed in the middle (MCA) and posterior cerebral artery (PCA) via transfer function phase and gain during respiratory-induced 0.1 Hz oscillations of arterial pressure. Within the patient group, 4 patients showed additional microbleeds in the basal ganglia on the MRI performed within the study (pure CAA vs mixed microbleeds). PCA phase was significantly lower in patients compared with controls (p = 0.018), particularly in patients with pure CAA (p = 0.0034). MCA values showed a similar but non-significant trend towards lower phase in patients with pure CAA. Poorer phase was associated with a higher number of microbleeds on MRI (MCA r = −0.57, p = 0.027; PCA r = −0.52, p = 0.098) and superficial cortical siderosis (PCA: p = 0.0025). In conclusion, dynamic cerebral autoregulation is impaired in patients with CAA. The degree of impairment is associated with the extent of cerebral microbleeds.
Stroke in the elderly
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CAA is an important cause of lobar intracerebral hemorrhage in the elderly and deserves further discussion (Viswanathan and Greenberg, 2011). CAA occurs in hereditary and sporadic forms (Gahr et al., 2013). Sporadic CAA is far more common and more likely to occur after the sixth decade, so we focus on the sporadic form in this section.
Stroke remains the second leading cause of death in the world, and its prevalence is projected to rise in the United States and globally. The main driver for increased stroke prevalence is aging of the population; however, best evidenced-based strategies for stroke treatment and prevention are not always followed for older patients. Furthermore, considerable gaps in knowledge exist for stroke prevention and treatment in elderly and very elderly patients.
In this chapter, we discuss various aspects of stroke care in the elderly, including the evidence that guides stroke prevention and treatment. We focus on the challenges in managing stroke in the very elderly including the paucity of data to guide management. The sections span the continuum of stroke care, from primary prevention to management of stroke complications. Finally, we highlight the most significant unanswered questions regarding stroke care in the elderly.
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Neuroimaging biomarkers for neurologic diseases are important tools, both for understanding pathology associated with cognitive and clinical symptoms and for differential diagnosis. This chapter explores neuroimaging measures, including structural and functional measures from magnetic resonance imaging (MRI) and molecular measures primarily from positron emission tomography (PET), in healthy aging adults and in a number of neurologic diseases. The spectrum covers neuroimaging measures from normal aging to a variety of dementias: late-onset Alzheimer's disease [AD; including mild cognitive impairment (MCI)], familial and nonfamilial early-onset AD, atypical AD syndromes, posterior cortical atrophy (PCA), logopenic aphasia (lvPPA), cerebral amyloid angiopathy (CAA), vascular dementia (VaD), sporadic and familial behavioral-variant frontotemporal dementia (bvFTD), semantic dementia (SD), progressive nonfluent aphasia (PNFA), frontotemporal dementia with motor neuron disease (FTD-MND), frontotemporal dementia with amyotrophic lateral sclerosis (FTD-ALS), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), dementia with Lewy bodies (DLB), Parkinson's disease (PD) with and without dementia, and multiple systems atrophy (MSA). We also include a discussion of the appropriate use criteria (AUC) for amyloid imaging and conclude with a discussion of differential diagnosis of neurologic dementia disorders in the context of neuroimaging.
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Cerebrovascular amyloidosis (CA) is a disease of the small blood vessels in the brain and is widely associated with both VaD and AD (Korczyn et al., 2012; Smith and Greenberg, 2009). CA is characterized by the deposition of Aβ plaques along the small arteries in the brain leading to changes in vascular lumen that may precipitate the onset of ischemia and hippocampal sclerosis (Gahr et al., 2013). The severity of cerebrovascular amyloid deposition has been linked to activity of several enzymes known to degrade amyloid peptides.
Diabetes mellitus (DM) is a major risk factor for Alzheimer's disease and vascular dementia. Few animal models exist that focus on the metabolic contributions to dementia onset and progression. Thus, there is strong scientific rationale to explore the effects of streptozotocin (STZ), a diabetogenic compound, on vascular and inflammatory changes within the brain.
The present study was designed to evaluate the effect of staggered, low-dose administration of STZ on behavioral and cognitive deficits, neuroinflammation, tau pathology, and histopathological alterations related to dementia.
Staggered administration (Days 1, 2, 3, 14, 15) of streptozotocin (40 mg/kg/mL) induced a diabetic-like state in mice, resulting in sustained hyperglycemia. STZ-treated animals displayed memory deficits in the novel object recognition task as well as increased tau phosphorylation and increased neuroinflammation. Additionally, STZ led to altered insulin signaling, exhibited by decreased plasma insulin and decreased levels of insulin degrading enzyme and pAKT within the hippocampus.
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Cerebral amyloid angiopathy-related cognitive impairment: The search for a specific neuropsychological pattern
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Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. CAA can also be diagnosed in memory clinics when patients are referred for cognitive impairment assessment, and may be a reason for admission to emergency or neurology departments because of rapidly progressive cognitive or neurological decline, or a transient focal neurological episode. CAA may even be observed in older community-dwelling individuals. Neuropsychological impairment in CAA has been described over the past 20 years. The symptoms most commonly reported are perceptual speed, episodic memory, semantic memory, attention and executive function, and global cognitive impairments. Psychiatric symptoms, such as personality changes, behavioral disturbances and depression, have been more recently described. CAA is also a risk factor for the development of dementia, and its relationship with Alzheimer's disease has been demonstrated in post-mortem studies. Yet, despite the increase in literature on CAA-related cognitive and psychiatric symptoms, the specific characteristics of symptoms in CAA are difficult to assess because of the substantial prevalence of comorbidities such as small vessel disease due to high blood pressure, Lewy body disease and, of course, AD, all of which act as important confounding factors. Also, within the entity of CAA itself, the additive and perhaps synergistic effects of each lesion on cognition remain to be assessed. In the present paper, the focus is on the latest evidence of neuropsychological impairment observed in CAA patients, and the emergence of a possible specific neuropsychological profile due to CAA is also discussed.

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ReviewCerebral amyloidal angiopathy—A disease with implications for neurology and psychiatry

Abstract

Introduction

Section snippets

Methods

Psychiatric implications of CAA

Conclusions

Acknowledgments

Depression after minor stroke: prevalence and predictors

Eur. J. Neurol.

Effects of peridopril-based lowering of blood pressure on intracerebral hemorrhage related to amyloid angiopathy: the PROGRESS trial

Stroke

Cerebral amyloid angiopathy pathology and cognitive domains in older persons

Ann. Neurol.

Sporadic cerebral amyloid angiopathy: pathology, clinical implications, and possible pathomechanisms

Acta Neuropathol.

Alzheimer's disease pathology influences severity and topographical distribution of cerebral amyloid angiopathy

Acta Neuropathol. (Berlin)

Unexpectedly low prevalence of intracerebral hemorrhages in sporadic cerebral amyloid angiopathy: an autopsy study

J. Neurol.

Review: sporadic cerebral amyloid angiopathy

Neuropathol. Appl. Neurobiol.

Imaging cerebral microbleeds using susceptibility weighted imaging: one step toward detecting vascular dementia

J. Magn. Reson. Imaging

Zerebrale Vaskulitis. In: Leitlinien für Diagnostik und Therapie in der Neurologie

Variants at APOE influence risk of deep and lobar intracerebral hemorrhage

Ann. Neurol.

Cerebral amyloid angiopathy: a systematic review

J. Clin. Neurol.

APOE genotype and extent of bleeding and outcome in lobar intracerebral haemorrhage: a genetic association study

Lancet Neurol.

Zerebrale Amyoloidangiopathie

Nervenarzt

Lobar hemorrhage in the elderly. The undiminishing importance of hypertension

Stroke

Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy

Nat. Rev. Neurosci.

Mechanisms of cerebrovascular amyloid deposition. Lessons from mouse models

Ann. N. Y. Acad. Sci.

Generation of beta-amyloid in the secretory pathway in neuronal and nonneuronal cells

Proc. Natl. Acad. Sci. USA

Cerebral beta amyloid angiopathy is a risk factor for cerebral ischemic infarction. A case control study in human brain biopsies

J. Neuropathol. Exp. Neurol.

Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid

Proc. Natl. Acad. Sci. USA

Intracerebral hemorrhage caused by cerebral amyloid angiopathy in a 53-year old man

J. Neurol.

Reversible leukoencephalopathy as a form of presentation in cerebral amyloid angiopathy

J. Neurol. Sci.

Alzheimer disease

Dis. Mon.

Transcriptomic and genetic studies identify IL-33 as a candidate gene for Alzheimer's disease

Mol. Psychiatry

Sporadic cerebral amyloid angiopathy revisited: recent insights into pathophysiology and clinical spectrum

J. Neurol. Neurosurg. Psychiatry

Cerebral amyloid angiopathy related inflammation: three case reports and a review

J. Neurol. Neurosurg. Psychiatry

Genetic-morphologic association study: association between the low density lipoprotein-receptor related protein (LRP) and cerebral amyloid angiopathy

Neuropathol. Appl. Neurobiol.

Current state and future directions of neurochemical biomarkers for Alzheimer's disease

Clin. Chem. Lab. Med.

Etude histochimique des plaques séniles

J. Belge Neurol. Psychiatry

Alzheimer's dementia by circulation disorders: when trees hide the forest

Nat. Cell Biol.

Increased frequency of the alpha-1-antichymotrypsin T allele in cerebral amyloid angiopathy

Neuropathology

Patient-specific decision-making for warfarin therapy in nonvalvular atrial fibrillation: how will screening with genetics and imaging help?

Stroke

Cerebral amyloid angiopathy in the brains of patients with Alzheimer's disease: the CREAD experience, Part XV

Neurology

Clinical manifestations of cerebral amyloid angiopathy-related inflammation

Ann. Neurol.

Cerebral amyloid angiopathy in dementia and old age

J. Neurol. Neurosurg. Psychiatry

Superficial siderosis of the central nervous system

Brain

Stroke related to cerebral amyloid angiopathy: the significance of systemic vascular disease

J. Neurol.

Human apolipoprotein E4 alters the amyloid-beta 40:42 ratio and promotes the formation of cerebral amyloid angiopathy in an amyloid precursor protein transgenic mouse model

Review
Cerebral amyloidal angiopathy—A disease with implications for neurology and psychiatry