scholarly journals Role of microglial amylin receptors in mediating beta amyloid (Aβ)-induced inflammation

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Wen Fu ◽  
Vlatka Vukojevic ◽  
Aarti Patel ◽  
Rania Soudy ◽  
David MacTavish ◽  
...  
Keyword(s):  
Beta Amyloid ◽  
Amyloid Aβ

scholarly journals The Function of Aβ in the Healthy Brain: Beta Amyloid as an Antimicrobial Protein

2021 ◽  
Vol 9 (9) ◽  
pp. 1250-1254
Author(s):  
Peter Iacobelli
Keyword(s):  
Beta Amyloid ◽  
Primary Objective ◽  
Synaptic Function ◽  
Antimicrobial Protein ◽  
Normal Brain ◽  
Aβ Peptides ◽  
Critical Studies ◽  
Amyloid Aβ ◽  
Objective Being

Abstract: There is no question as to whether or not the beta amyloid (Aβ) peptide plays a role in the exacerbation and onset of AD. There are very evident correlations between the volume of Aβ deposition in the AD brain and the severity of the symptoms of AD-typical neurodegeneration. There are certainly many factors involved in the progression of AD, of which the aggregation of Aβ peptides is only one. While many have ruminated on the mechanism by which Aβ serves to impair synaptic function and contribute to neurodegeneration, the role of this protein has yet to be fully uncovered, not just in the AD brain, but in the normally functioning brain as well. Recent research has shed light on the role of Aβ in the normal brain, offering evidence for the fact that beta amyloid functions as an antimicrobial protein, with its primary objective being to serve an immunoresponsive purpose. This text will highlight some of the critical studies on the topic, and illuminate the role that Aβ most likely plays in the functioning of the normal brain, and how this influences its pathological deposition in the AD brain.

scholarly journals Clearance of beta-amyloid is facilitated by apolipoprotein E and circulating high-density lipoproteins in bioengineered human vessels

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jerome Robert ◽  
Emily B Button ◽  
Brian Yuen ◽  
Megan Gilmour ◽  
Kevin Kang ◽  
...  
Keyword(s):  
Vascular Tissue ◽  
Density Lipoprotein ◽  
Beta Amyloid ◽  
High Density ◽  
Cerebral Vessels ◽  
High Density Lipoproteins ◽  
Amyloid Angiopathy ◽  
Dementia Risk ◽  
Amyloid Aβ

Amyloid plaques, consisting of deposited beta-amyloid (Aβ), are a neuropathological hallmark of Alzheimer’s Disease (AD). Cerebral vessels play a major role in AD, as Aβ is cleared from the brain by pathways involving the cerebrovasculature, most AD patients have cerebrovascular amyloid (cerebral amyloid angiopathy (CAA), and cardiovascular risk factors increase dementia risk. Here we present a notable advance in vascular tissue engineering by generating the first functional 3-dimensioinal model of CAA in bioengineered human vessels. We show that lipoproteins including brain (apoE) and circulating (high-density lipoprotein, HDL) synergize to facilitate Aβ transport across bioengineered human cerebral vessels. These lipoproteins facilitate Aβ42 transport more efficiently than Aβ40, consistent with Aβ40 being the primary species that accumulates in CAA. Moreover, apoE4 is less effective than apoE2 in promoting Aβ transport, also consistent with the well-established role of apoE4 in Aβ deposition in AD.

scholarly journals Inflammation in Alzheimer’s disease: A friend or foe?

2018 ◽  
Vol 5 (8) ◽  
pp. 2552-2564 ◽  
Author(s):  
Samaila Musa Chiroma ◽  
Mohamad Taufik Hidayat Baharuldin ◽  
Che Norma Mat Taib ◽  
Zulkhairi Amom ◽  
Saravanan Jagadeesan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Aβ Peptide ◽  
Cellular Mechanisms ◽  
Scientific Databases ◽  
Amyloid Aβ ◽  
The Brain ◽  
Convincing Data

Background: There is a dearth of precise information for molecular and cellular mechanisms responsible for the development of Alzheimer’s disease (AD). However, convincing data from clinical research and basic molecular biology have shown that inflammation of the brain is an integral part of AD. In this review, the role of inflammation in AD will be highlighted. Methods: Articles from credible scientific databases, such as ScienceDirect, Scopus, PubMed, Google Scholar and Mendeley, were searched and retrieved using keywords ‘inflammation’, ‘Alzheimer’s disease’, ‘tau’, and ‘beta amyloid’. Results: At present, there is no local inflammatory-inciting factor that is closely associated with AD, although it has been proposed that inflammation could be induced by pathologic hallmarks of AD, such as beta amyloid (Aβ) peptide plagues and neurofibrillary tangles (NFTs), or fragments of degenerated neurons. However, it is still unclear whether inflammation leads to the development of AD or if the pathological hallmarks of AD induce inflammation. Conclusion: Inflammation is, indeed, an integral part of AD. Further studies on inflammatory-targeted therapies for AD are highly recommended.

Exploring the Role of Aggregated Proteomes in the Pathogenesis of Alzheimer’s Disease

2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Early Onset ◽  
Late Onset ◽  
Precursor Protein ◽  
Brain Disorder ◽  
Amyloid Aβ ◽  
T Tau

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.

Understanding the structural requirements of cyclic sulfone hydroxyethylamines as hBACE1 inhibitors against Aβ plaques in Alzheimer's disease: a predictive QSAR approach

RSC Advances ◽  
2016 ◽  
Vol 6 (34) ◽  
pp. 28171-28186 ◽  
Author(s):  
Pravin Ambure ◽  
Kunal Roy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Beta Amyloid ◽  
Precursor Protein ◽  
Structural Requirements ◽  
Amyloid Aβ

Beta (β)-site amyloid precursor protein cleaving enzyme 1 (BACE1) is one of the most important targets in Alzheimer's disease (AD), which is responsible for production and accumulation of beta amyloid (Aβ).

P4-287: The role of microglia in BETA-AMYLOID immunotherapy

2012 ◽  
Vol 8 (4S_Part_21) ◽  
pp. S759-S759
Author(s):  
Gina Eom ◽  
Stefan Prokop ◽  
Frank L Heppner
Keyword(s):  
Beta Amyloid

scholarly journals Improvement of glymphatic-lymphatic drainage of beta-amyloid by focused ultrasound in Alzheimer’s disease model

2020 ◽  
Author(s):  
Youngsun Lee ◽  
Yoori Choi ◽  
Eun-Joo Park ◽  
Seokjun Kwon ◽  
Hyun Kim ◽  
...  
Keyword(s):  
Focused Ultrasound ◽  
Disease Model ◽  
Early Period ◽  
Beta Amyloid ◽  
Lymphatic Drainage ◽  
Beneficial Effects ◽  
Age Related ◽  
Early Dementia ◽  
Amyloid Aβ ◽  
Brain Homeostasis

AbstractDrainage of parenchymal waste through the lymphatic system maintains brain homeostasis. Age-related changes of glymphatic-lymphatic clearance lead to the accumulation beta-amyloid (Aβ) in dementia models. In this study, focused ultrasound treatment in combination with microbubbles (FUS-MB) improved Aβ drainage in early dementia model mice, 5XFAD. FUS-MB enhanced solute Aβ clearance from brain, but not plaques, to cerebrospinal fluid (CSF) space and then deep cervical lymph node (dCLN). dCLN ligation exaggerated memory impairment and progress of plaque formation and also the beneficial effects of FUS-MB upon Aβ removal through CSF-lymphatic routes. In this ligation model, FUS-MB improved memory despite accumulation of Aβ in CSF. In conclusion, FUS-MB enhances glymphatic-lymphatic clearance of Aβ mainly by increasing brain-to-CSF Aβ drainage. We suggest that FUS-MB can delay dementia progress in early period and benefits of FUS-MB depend on the effect of Aβ disposal through CSF-lymphatics.

Sign in / Sign up

Export Citation Format

Share Document