Neurology: Patients with amyloid vascular disease, memory deterioration may reflect tau pathology

Cerebral amyloid vascular disease (CAA) is a kind of amyloid deposition in the meningeal and cortical microvascular blood vessel disease that is characterized, vascular cognitive impairment and is a critical factor leading to dementia.
Although CAA is a common concomitant feature of Alzheimer's disease (AD), it is an independent neuropathological condition, and more than half of CAA cases are not accompanied by AD-related tau pathology.
Clinically, distinguishing CAA patients with or without tau pathology is of great significance to the treatment and prognosis.

Blood vessel

Previous studies on patients with Alzheimer's disease have shown that memory performance is closely related to the severity of tau-mediated neuropathological changes in the medial temporal lobe, and can predict impending cognitive decline.
In view of this evidence, the existence of objective memory impairment in CAA patients can provide relevant information about the underlying neuropathological process and suggest the accompanying increase in the severity of tau pathology.

In this way, Dorothee Schoemaker of Harvard Medical School used tau-PET imaging to explore whether memory impairment is related to tau lesions in patients with cerebral amyloid angiopathy (CAA).

They included 46 patients who may have CAA underwent neuropsychological examinations and MRI to quantify structural markers of cerebral small vessel disease.
Some of these participants also completed [11C]-Pittsburgh compound B (n = 39) and [18F]-flortaucipir (n = 40) PET, which were used to estimate amyloid and tau burden, respectively.

Based on neuropsychological performance, participants were divided into amnesia and non-amnesia.
Statistical analysis was performed to examine the differences in cognitive ability, structural markers of cerebral small vessel disease, and retention of amyloid and tau-PET between CAA participants with and without amnesia.

They found that , compared with non-amnesia patients, patients with probable CAA and memory loss showed overall more severe cognitive impairment, smaller hippocampal volume (p <0.
001), and susceptibility to Alzheimer’s Areas affected by Murer's neurodegeneration increased tau-PET binding (p = 0.
003).

Compared with non-amnesia patients, patients with probable CAA and memory loss showed overall more severe cognitive impairment and smaller hippocampal volume (p <0.
001), and patients with probable CAA and memory loss Compared with non-amnesia patients, patients with performance showed more severe cognitive impairment and smaller hippocampal volume (p <0.
001),

There was no difference in any other MRI markers or amyloid-PET binding between the amnesiac and non-amnesia patients with CAA.
In the generalized linear model of all neuroimaging markers evaluated, tau-PET (β = -0.
85, p = 0.
001) and hippocampal volume (β = 0.
64 p = 0.
01) were the only important factors predicting memory performance.
Among the cognitive characteristics of CAA patients, patients with elevated Tau-PET had significantly lower performance in the memory field (P = 0.
004).

The important significance of this study lies in the discovery that there is objective memory impairment in probable CAA patients, which can be used as a sign of potential tau disease .

There is objective memory impairment in probable CAA patients, which can be used as a sign of potential tau disease .
There is objective memory impairment in probable CAA patients, which can be used as a sign of potential tau disease

Original source: neurology.

org/content/96/15/e1975" target="_blank" rel="noopener">Schoemaker, Dorothee et al "Association of Memory Impairment With Concomitant Tau Pathology in Patients With Cerebral Amyloid Angiopathy.
" Neurology 96.

neurology.
org/content/96/15/e1975" target="_blank" rel="noopener">Schoemaker, Dorothee et al "Association of Memory Impairment With Concomitant Tau Pathology in Patients With Cerebral Amyloid Angiopathy.
" Neurology 96.
15 (2021): e1975-e1986.
Web.
28 April.
2021.
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