Senile plaque calcification of the lamina circumvoluta medullaris in Alzheimer's disease

Schober, R.; Hilbrich, Isabel; Jäger, Carsten; Holzer, Max

doi:10.1111/neup.12742

Cited by 3 publications

(4 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the aged hippocampus, arteries, pre-capillaries and capillaries were calcified ( Peters et al, 2018 ). Similar calcification of hippocampal vessels has been reported in AD patients ( Wegiel et al, 2002 ; Schober et al, 2021 ). A recent study showed that the tunica media of arterioles in the globus pallidus is calcified in aged individuals, confirmed both histologically and on CT. Calcification of the vascular tree showed a distribution pattern, starting in the ventral striatopallidum spreading posterolaterally into the external half of the globus pallidus ( de Brouwer et al, 2021 ).…”

Section: Bone In the Brain—an Overview Of Cerebrovascular Calcificationssupporting

confidence: 84%

“…There is differential involvement of the vascular tree (artery, capillary), which might be dependent on the anatomical region and underlying disease. For example, previous histopathological studies detected arterial calcification in aged subjects and AD patients compared to capillary bed calcification in the globus pallidus in Down syndrome patients ( Wegiel et al, 2002 ; Schober et al, 2021 ).…”

Section: Bone In the Brain—an Overview Of Cerebrovascular Calcificationsmentioning

confidence: 99%

See 1 more Smart Citation

The Interplay Between Brain Vascular Calcification and Microglia

Maheshwari

Huang

Sridhar

et al. 2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

Vascular calcifications are characterized by the ectopic deposition of calcium and phosphate in the vascular lumen or wall. They are a common finding in computed tomography scans or during autopsy and are often directly related to a pathological condition. While the pathogenesis and functional consequences of vascular calcifications have been intensively studied in some peripheral organs, vascular calcification, and its pathogenesis in the central nervous system is poorly characterized and understood. Here, we review the occurrence of vessel calcifications in the brain in the context of aging and various brain diseases. We discuss the pathomechanism of brain vascular calcification in primary familial brain calcification as an example of brain vessel calcification. A particular focus is the response of microglia to the vessel calcification in the brain and their role in the clearance of calcifications.

show abstract

Section: Bone In the Brain—an Overview Of Cerebrovascular Calcificationssupporting

confidence: 84%

Section: Bone In the Brain—an Overview Of Cerebrovascular Calcificationsmentioning

confidence: 99%

The Interplay Between Brain Vascular Calcification and Microglia

Maheshwari

Huang

Sridhar

et al. 2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

show abstract

“…It is well known that calcification of blood vessels is associated with vascular ageing and atherosclerosis, adding further evidence that atherosclerosis might be an early event in Alzheimer's disease development. To our knowledge, a previous published case report also linked vessel calcification with Alzheimer's disease [29].…”

Section: Resultsmentioning

confidence: 99%

Senile plaques in Alzheimer's disease arise from Aβ‐ and Cathepsin D‐enriched mixtures leaking out during intravascular haemolysis and microaneurysm rupture

et al. 2022

FEBS Letters

View full text Add to dashboard Cite

Senile plaques are a pathological hallmark of Alzheimer's disease (AD), yet the mechanism underlying their generation remains unknown. Beta‐amyloid peptide (Aβ) is a major component of senile plaques. We analysed AD brain tissues with histochemistry, immunohistochemistry and fluorescence imaging to examine the neural, vascular or blood Aβ contribution to senile plaque development. We found little neural marker co‐expression with plaque Aβ, while co‐expression of blood markers, such as Haemin and ApoE, was abundant. The plaque cores were structured with vascular and glial proteins outside and blood metabolites inside, co‐localizing with a characteristic of Hoechst staining‐independent blue autofluorescence. Erythrocyte‐interacting Aβ is linked to coagulation, elevated calcium and blue autofluorescence, and it is associated with intravascular haemolysis, atherosclerosis, cerebral amyloid angiopathy, microaneurysm, and often with Cathepsin D co‐expression. We identified microaneurysms as major sites of amyloid formation. Our data suggest that senile plaques arise from Aβ‐ and Cathepsin D‐enriched mixtures leaking out during intravascular haemolysis and microaneurysm rupture.

show abstract

“…Recent investigations have brought to light a significant association between a hereditary variant of CAA, known as the Dutch type, and IAC [189] . Studies have revealed a connection between osteopontin (OPN), and the TGFβ1/phospho-SMAD2/3 signaling pathway in calcified arteries affected by hereditary CAA [190,191] . Interestingly, the researchers observed a correlation between the pro-calcific accumulation of collagen 1, OPN, and the activation of the pSMAD2/3 pathway with the severity of CAA.…”

Section: Co-occurrence Of Calcification and Amyloidmentioning

confidence: 99%

Extracellular vesicles: the key to unlocking mechanisms of age-related vascular disease?

Whitehead,

Antonazzi,

Shanahan

2024

J Cardiovasc Aging

View full text Add to dashboard Cite

Aging is associated with the development of two ubiquitous, detrimental pathologies, vascular calcification and amyloidosis. These pathologies are characterized by the accumulation of toxic aggregates in the vessel extracellular matrix (ECM) in the form of crystalline calcium and phosphate mineral or insoluble protein fibrils, respectively. These aggregates impact ECM integrity, drive vascular stiffening, and can also cause cell death and phenotypic change in the cells that interact with them. The deposition of both calcification and amyloid requires a nucleus that can mediate the mineralization of calcium and phosphate, or amyloid aggregation from precursor proteins or peptides. Emerging evidence suggests that changes in the composition of the ECM associated with cellular senescence, as well as extracellular vesicle (EV) release, cargo-loading, trapping, and aggregation within the ECM, are common and synergistic mechanisms that regulate the development of these pathologies. Importantly, vascular smooth muscle cells (VSMCs) orchestrate the formation of both pathologies that commonly co-occur in the aging vasculature. Here, we outline the commonalities and differences in what is known about the genesis of calcification and amyloid, and highlight key questions and areas that remain unknown and require further investigation. The complex relationship between senescence, EVs, and the ECM, mediated by VSMCs, which drives the accumulation of HA and amyloid, could be a target for therapeutic intervention.

show abstract

Senile plaque calcification of the lamina circumvoluta medullaris in Alzheimer's disease

Cited by 3 publications

References 21 publications

The Interplay Between Brain Vascular Calcification and Microglia

The Interplay Between Brain Vascular Calcification and Microglia

Senile plaques in Alzheimer's disease arise from Aβ‐ and Cathepsin D‐enriched mixtures leaking out during intravascular haemolysis and microaneurysm rupture

Extracellular vesicles: the key to unlocking mechanisms of age-related vascular disease?

Contact Info

Product

Resources

About