Title:Neuropsychological Aspects of Sporadic Cerebral Amyloid Angiopathy: A Case Series and Narrative Review
Volume: 22
Issue: 8
Author(s): Luca Pizzoni*, Andrea Cavalli, Federica Di Matteo and Giovanni Mancini
Affiliation:
- Centre for Cognitive Disorders and Dementia (CDCD), ASL Roma 3, 00122 Rome, Italy
- PhD Program in Behavioral Neuroscience, "La Sapienza" University of Rome, 00185 Rome, Italy
Keywords:
Cerebral amyloid angiopathy, Alzheimer’s disease, cognitive impairment, amyloid-β protein, neuropsychological assessment, cerebral small vessel disease, cerebrovascular disorders.
Abstract:
Introduction: Cerebral Amyloid Angiopathy (CAA) is a common form of cerebral small
vessel disease (CSVD), characterized by the accumulation of amyloid-β (Aβ) protein in the walls of
cortical and leptomeningeal arteries and arterioles. The sporadic form primarily affects the elderly
and is closely associated with Alzheimer’s disease (AD). Despite previous studies on cognition, the
specific neuropsychological profile of CAA remains unclear. This study aims to describe the cognitive
profile of CAA patients and characterize their neuropsychological aspects in the absence of a
clinical diagnosis of AD.
Methods: We present a case series of six patients with probable CAA, without clinical evidence of
AD, who underwent extensive neuropsychological assessment. Additionally, a narrative review was
conducted to synthesize current knowledge of the cognitive and neuropsychological aspects of sporadic
CAA.
Results: The narrative review indicates that CAA predominantly affects executive functioning, processing
speed, episodic memory, global cognition, and visuospatial functions. In our case series, all
patients exhibited impairments in these domains, except for global cognition. Notably, a specific
dissociation was observed in the Rey Auditory Verbal Learning Test (RAVLT), with impaired delayed
recall but preserved recognition.
Discussion: Sporadic CAA in patients without AD contributes to cognitive impairment, particularly
affecting executive functioning, processing speed, visuospatial functions, and episodic memory. In
our sample, memory impairment in CAA follows a dysexecutive pattern, characterized by retrieval
deficits with preserved storage. This contrasts with the amnestic profile seen in AD and amnestic
mild cognitive impairment (aMCI), where both retrieval and storage are compromised.
Conclusion: This distinct memory profile may represent a useful neuropsychological marker for
differentiating CAA-related cognitive impairment from that associated with AD and its prodromal
forms. This differentiation has potential implications for diagnosis, prognosis, and the development
of tailored therapeutic strategies.
