The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma.

In the paper

“The brain and retina are affected in several neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and glaucoma.”

In the paper

“they have similar mechanisms of cell injury and deposition of protein aggregates in specific anatomical areas (Wostyn et al., 2010; Kaarniranta et al., 2011; Ghiso et al., 2013)”

What the sources say

• Not checked yetcites Wostyn et al., 2010 source
• Not checked yetcites Kaarniranta et al., 2011 source
• Not checked yetcites Ghiso et al., 2013 source

In the paper

“These neurodegenerative diseases share a common pathogenic mechanism, the neuroinflammation, in which microglia play an important role.”

In the paper

“In addition, AD is frequently associated with vascular dysfunctions and inflammation (Dudvarski Stankovic et al., 2016).”

What the sources say

• Not checked yetcites Dudvarski Stankovic et al., 2016 source

In the paper

“The loss of neurons is accompanied by abnormal intracytoplasmic filamentous aggregates called Lewy bodies.”

In the paper

“These aggregates (deposited in somas and axons) are constituted by α-syn, parkin, phosphorylated neurofilament and components of the protheosomic-ubiquitin pathway (Orr et al., 2002).”

What the sources say

• Not checked yetcites Orr et al., 2002 source

In the paper

“they are slow and chronic neurodegenerative disorders with a strong age-related incidence”

In the paper

“Microglia, the immunocompetent cells of the central nervous system (CNS), act as neuropathology sensors and are neuroprotective under physiological conditions.”

In the paper

“The major pathology related to AD is the extracellular deposit of β-amyloid (Aβ) in the form of parenchymal plaques and cerebral amyloid angiopathy co-existing with intraneuronal accumulations of hyperphosphorylated tau (pTau) (neurofribillary tangles) (Ghiso et al., 2013).”

What the sources say

• Not checked yetcites Ghiso et al., 2013 source

In the paper

“AD has been related to genetic mutations, among them in the gene encoding the Aβ precursor protein peptide, mutations in the presenilins genes (Calabrese et al., 2001) and the presence of the APOE ε4 allele (Martínez-Lazcano et al., 2010).”

What the sources say

• Not checked yetcites Calabrese et al., 2001 source
• Not checked yetcites Martínez-Lazcano et al., 2010

In the paper

“Genetic factors include mutations in α-syn (Olanow and Tatton, 1999; Pérez and Arancibia, 2007), while mitochondrial dysfunction and oxidative stress may also act by causing the accumulation of misfolded proteins (Dauer and Przedborski, 2003).”

What the sources say

• Not checked yetcites Olanow and Tatton, 1999
• Not checked yetcites Pérez and Arancibia, 2007
• Not checked yetcites Dauer and Przedborski, 2003 source

In the paper

“Neurodegeneration could be due to exposure to dopaminergic neurotoxins e.g., herbicides (MPTP), insecticides (Rotenone), and metals (Hernández-Montiel, 2006).”

What the sources say

• Not checked yetcites Hernández-Montiel, 2006

In the paper

“The clinical symptoms of PD are mainly motor problems, including bradykinesia, rigidity, tremors, and postural instability. In addition, PD presents non-motor symptoms including disorganized speech and altered moods (Fakhoury, 2016).”

What the sources say

• Not checked yetcites Fakhoury, 2016 source

In the paper

“AD is an age-related neurodegeneration of the CNS characterized by neuronal and synaptic loss in the cerebral cortex, resulting in cognitive deficit and dementia.”

In the paper

“Recently, neurodegenerative lesions have been detected in the intracranial optic nerve, the lateral geniculate nucleus, and the visual cortex (Gupta et al., 2006, 2007), suggesting that this pathology could be grouped as a neurodegenerative disease (Yucel et al., 2003).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Gupta et al., 2006, 2007
• Not checked yetcites Yucel et al., 2003 source

In the paper

“The main etiological factors proposed for PD are aging, environmental toxins, and genetic factors.”

In the paper

“AD involves progressive memory loss and dementia (Sharma and Lipincott, 2017)”

What the sources say

• Not checked yetcites Sharma and Lipincott, 2017

In the paper

“PD is a neurodegenerative locomotor disorder with the progressive loss of dopaminergic neurons in the substantia nigra.”

In the paper

“Glaucoma is a multifactorial neurodegenerative disease of the optic nerve, characterized by retinal ganglion cell loss.”

In the paper

“The activated microglia can release pro-inflammatory cytokines which can aggravate and propagate neuroinflammation, thereby degenerating neurons and impairing brain as well as retinal function.”

In the paper

“while the PD is a chronic and progressive movement disorder (Orr et al., 2002).”

What the sources say

• Not checked yetcites Orr et al., 2002 source

In the paper

“The extracellular deposits of beta-amyloid (Aβ) and intraneuronal accumulations of hyperphosphorylated tau protein (pTau) are the hallmarks of this disease.”

In the paper

“Alzheimer's Disease (AD) and Parkinson's Disease (PD) are the most common neurodegenerative disorders (de Lau and Breteler, 2006).”

What the sources say

• Not checked yetcites de Lau and Breteler, 2006 source

In the paper

“Glaucoma is an age-related multifactorial neurodegenerative disease of the optic nerve, with an irreversible decrease in RGCs, causing a visual-field loss and cupping of the optic nerve head (Quigley et al., 1988).”

What the sources say

• Not checked yetcites Quigley et al., 1988 source

In the paper

“A neuroinflammatory response is considered among the etiological factors of the major aged-related neurodegenerative diseases of the CNS, and microglial cells are key players in these neurodegenerative lesions.”

In the paper

“This is accompanied by Lewy body inclusion composed of α-synuclein (α-syn) aggregates.”

In the paper

“However, it is now known to have a multifactorial origin and it seems to result from a complex interaction of multiple environmental and genetic factors (Wostyn et al., 2010).”

What the sources say

• Not checked yetcites Wostyn et al., 2010 source

In the paper

“These deposits are also found in the retina and optic nerve.”

In the paper

“In glaucoma, increased intraocular pressure (IOP), vascular dysregulation, and the immune system activation can trigger several changes in retina and optic nerve including: disrupted axonal transport and neurofilament accumulation, microvascular abnormalities, extracellular matrix remodeling, and glial cell activation.”

In the paper

“Microglia react to injury and degeneration with immune-phenotypic and morphological changes, proliferation, migration, and inflammatory cytokine production.”

In the paper

“PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the nerve terminals in the striatum (Dauer and Przedborski, 2003).”

What the sources say

• Not checked yetcites Dauer and Przedborski, 2003 source

In the paper

“PD also involves retinal dopaminergic cell degeneration.”

In the paper

“Excessive microglia activation might prompt the release of cytotoxic factors, causing neuronal damage, which could accelerate the progression of some CNS diseases.”

In the paper

“The second microglial phenotype, M2-like, secrete anti-inflammatory mediators and neurotrophic factors, thus inducing a supportive microenvironment for neurons (Kettenmann et al., 2011).”

What the sources say

• Not checked yetcites Kettenmann et al., 2011 source

In the paper

“Changes in OCT measurements have been used to study the course of particular neurologic diseases such AD (Garcia-Martin et al., 2014; Maldonado et al., 2015; Salobrar-Garcia et al., 2015, 2016a,b), PD (Yu et al., 2014; Stemplewitz et al., 2015; Boeke et al., 2016; Satue et al., 2017), and glaucoma (Leung, 2016; Fallon et al., 2017), suggesting that the data compiled may be useful as a biomarker in”

What the sources say

• Not checked yetcites Garcia-Martin et al., 2014 source
• Not checked yetcites Yu et al., 2014
• Not checked yetcites Leung, 2016 source

In the paper

“The fractalkine expressed by neurons can induce adenosine release from microglia. This adenosine (via adenosine A1 receptor) can activate survival pathways in neurons sensitive to excitotoxicity challenge (Lauro et al., 2008, 2010).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lauro et al., 2008, 2010

In the paper

“Microglia constitute the first line of immune defense in CNS.”

In the paper

“Thus, it has been described that the retina is a “window to the brain,” and the manifestation of disease in the brain is the same as in the retina (MacCormick et al., 2015).”

What the sources say

• Not checked yetcites MacCormick et al., 2015 source

In the paper

“These microvesicles are involved in all immune activities and can be protective or detrimental, affecting some pathologies of the CNS.”

In the paper

“However, in certain circumstances, the neuroinflammation can help stimulate myelin repair or remove toxic aggregated proteins and cell debris from CNS (Ding et al., 2004; Simard et al., 2006; Glezer et al., 2007).”

What the sources say

• Not checked yetcites Ding et al., 2004 source
• Not checked yetcites Simard et al., 2006 source
• Not checked yetcites Glezer et al., 2007 source

In the paper

“Although the exact mechanism bringing about this neuronal death remains unknown, these neurodegenerative disorders seem to have pathogenic mechanisms in common.”

In the paper

“These cells survey the CNS in order to detect homeostasis alteration and they respond accordingly, combining a defensive service with neuroprotective functions (Verkhratsky and Butt, 2013).”

What the sources say

• Not checked yetcites Verkhratsky and Butt, 2013

In the paper

“The change of microglia between M1 and M2 phenotypes is a dynamic process and microglial activation can switch from M2 to M1 phenotype during the course of disease (Cherry et al., 2014).”

What the sources say

• Not checked yetcites Cherry et al., 2014 source

In the paper

“The morphology of activated microglia includes a retraction of processes, enlargement of the soma, and increased expression of myeloid cell markers (Ransohoff and Cardona, 2010).”

What the sources say

• Not checked yetcites Ransohoff and Cardona, 2010 source

In the paper

“After this acute M1 activation, microglial cells can suffer an uncontrolled activation leading to a state of chronic inflammation. In this state, microglia release neurotoxic inflammatory factors (TNF-α, IL-1α, IL-1β, IL-6, NO, hydrogen peroxide, superoxide anion, chemokines, and glutamate), which lead to neuronal death (Block et al., 2007; Lull and Block, 2010; Burguillos et al., 2011; Kettenmann”

What the sources say

• Not checked yetcites Block et al., 2007 source
• Not checked yetcites Lull and Block, 2010 source
• Not checked yetcites Burguillos et al., 2011 source

In the paper

“M1 microglial cells present amoeboid morphology as well as high phagocytic capacity and motility (Varnum and Ikezu, 2012; Gonzalez et al., 2014; Jones and Bouvier, 2014).”

What the sources say

• Not checked yetcites Varnum and Ikezu, 2012
• Not checked yetcites Gonzalez et al., 2014 source
• Not checked yetcites Jones and Bouvier, 2014

In the paper

“The neuroinflammatory process occurs not only in the brain, but also in the retina, which is a projection of the CNS.”

In the paper

“EVs have a heterogeneous molecular composition, including receptors, integrins and cytokines, bioactive lipids, miRNA, mRNA, DNA, and organelles, being similar to their parental cells.”

In the paper

“M2 microglia are the major effector cells with the potential to dampen pro-inflammatory immune responses and promote the expression of repair genes (Tang and Le, 2016).”

What the sources say

• Not checked yetcites Tang and Le, 2016 source

In the paper

“Microglial cells are CNS resident immune cells which have sensor and effector functions as well as phagocytic capacity (Streit et al., 2005).”

What the sources say

• Not checked yetcites Streit et al., 2005 source

In the paper

“The retina and brain are associated over a range of neurological and neurovascular conditions of varying etiologies, because the retina and brain are similar, and respond similarly to disease.”

In the paper

“Microglial cells may undergo two different kinds of activation in response to infections or injuries. The first is a neurotoxic phenotype called M1-like.”

In the paper

“After injury these cells become activated and in this state change their morphology, proliferate, migrate to the damage sites, modify the expression of enzymes and receptors, and release a variety of inflammatory factors, such as NO, tumor necrosis factor (TNF-α), interleukin (IL-6) among others (Magni et al., 2012).”

What the sources say

• Not checked yetcites Magni et al., 2012 source

In the paper

“These cells can release anti-inflammatory cytokines including IL-4, IL-13, IL-10, TGF-β and neurotrophic factors, such as insulin-like growth factor 1 (IGF-1) to assist inflammation resolution and promote neuron survival (Suh et al., 2013; Tang and Le, 2016).”

What the sources say

• Not checked yetcites Suh et al., 2013 source
• Not checked yetcites Tang and Le, 2016 source

In the paper

“Neuroinflammation, the inflammation of central nervous system (CNS), is essential to protect the tissue. However, uncontrolled and prolonged neuroinflammation is potentially harmful and can cause cellular damage.”

In the paper

“Fractalkine, involved in indirect neuroprotection, is released by neurons and the receptor is expressed by microglia, their interactions constituting a neuron-microglial signaling system (Ransohoff and El Khoury, 2015).”

What the sources say

• Not checked yetcites Ransohoff and El Khoury, 2015 source

In the paper

“Microglia express CD11b/c, D45low, and the chemokine fractalkine receptor (CX3CR1) (Dudvarski Stankovic et al., 2016).”

What the sources say

• Not checked yetcites Dudvarski Stankovic et al., 2016 source

In the paper

“The microglial EVs representing a “liquid biopsy” of their parental cells, and could provide information on the functional phenotype (protective or damaging) of microglial cells over the course of neurodegeneration (Nigro et al., 2016).”

What the sources say

• Not checked yetcites Nigro et al., 2016 source

In the paper

“After injury, astrocytes produce cytokines and chemokines (CCL2, CXCL1, CXCL10, GM-CSF, and IL-6), which activate microglia and recruit peripheral immune cells to the CNS.”

In the paper

“Microglia and astrocytes are the main innate immune effector cells in the CNS (da Fonseca et al., 2014).”

What the sources say

• Not checked yetcites da Fonseca et al., 2014 source

In the paper

“death occurs in one or more populations of neurons (RGCs in glaucoma, hippocampal and cortical neurons in AD and nigrostriatal dopaminergic neurons in PD) (Mattson, 2000).”

What the sources say

• Not checked yetcites Mattson, 2000 source

In the paper

“In their state of high activation, microglial cells acquire an amoeboid morphology and act like macrophages, engulfing debris (Brown and Neher, 2014).”

What the sources say

• Not checked yetcites Brown and Neher, 2014 source

In the paper

“All this could generate oxidative stress, which leads to neuronal death.”

In the paper

“Microglia, together with endothelial cells, pericytes, and astrocytes, form the functional blood-brain barrier (BBB) that selectively separates the brain parenchyma from blood circulation.”

In the paper

“Their assembly and activation regulates activation of caspase-1, which catalyzes the cleavage and activation of proinflammatory cytokines of the IL-1β family, promoting the secretion of these, now biologically active, cytokines. These cytokines could induce neuronal degeneration (Gold and El Khoury, 2015).”

What the sources say

• Not checked yetcites Gold and El Khoury, 2015 source

In the paper

“The activated microglia can induce the dysfunction of the BBB, being correlated with the disruption of the BBB in the neurodegenerative diseases (Dudvarski Stankovic et al., 2016).”

What the sources say

• Not checked yetcites Dudvarski Stankovic et al., 2016 source

In the paper

“This pathway plays a critical role in the initiation and regulation of innate immune responses and adaptive immunity (Yan et al., 2016).”

What the sources say

• Not checked yetcites Yan et al., 2016 source

In the paper

“This model postulates that the initial deposition of Aβ triggers mechanisms that progressively lead to Tau pathology, synaptic dysfunction, inflammation, neuronal loss and finally to dementia (De Strooper and Karran, 2016).”

What the sources say

• Not checked yetcites De Strooper and Karran, 2016 source

In the paper

“As mentioned above, for phagocytosis to occur the expression of specific receptors on the microglial surface is necessary. The principal receptors are the TLRs, which have high affinity for pathogens, and TREM2, which recognizes apoptotic cellular substances (Hsieh et al., 2009).”

What the sources say

• Not checked yetcites Hsieh et al., 2009 source

In the paper

“The complement also participates in the physiological process, termed synaptic pruning. The synapses and axons have to be labeled by complement components C1q and C3 before being phagocytosed, which prompts their selective recognition by microglial cells (Paolicelli et al., 2011; Linnartz et al., 2012; Schafer et al., 2012).”

What the sources say

• Not checked yetcites Paolicelli et al., 2011 source
• Not checked yetcites Linnartz et al., 2012 source
• Not checked yetcites Schafer et al., 2012 source

In the paper

“This pathway constitutes a pattern-recognition system by which microglial cells respond to foreign antigens and inflammation in the CNS (Hanisch and Kettenmann, 2007).”

What the sources say

• Not checked yetcites Hanisch and Kettenmann, 2007 source

In the paper

“The RAGE is an important cell-surface receptor for Aβ in the endothelial cells, neurons, and microglia, and increased expression in these cell types has been demonstrated in AD (Yan et al., 1996).”

What the sources say

• Not checked yetcites Yan et al., 1996 source

In the paper

“Activated microglia can induce A1 astrocytes by secreting IL-1α, TNF, and C1q, and this type of astrocyte contribute to the death of neurons in the neurodegenerative disorders and could be analog to the M1-like phenotype microglia (Liddelow et al., 2017).”

What the sources say

• Not checked yetcites Liddelow et al., 2017 source

In the paper

“This inflammation not only occurs in response to Aβ deposition, but is also capable of generating, via feedback mechanisms, more Aβ while weakening the mechanisms responsible for its elimination (Parpura et al., 2012).”

What the sources say

• Not checked yetcites Parpura et al., 2012 source

In the paper

“The primary pathogenic process in AD is the accumulation of Aβ protein. This protein aggregates into extracellular amyloid plaques, which are the hallmark of this pathology (Southam et al., 2016).”

What the sources say

• Not checked yetcites Southam et al., 2016 source

In the paper

“This receptor is a critical regulator of microglia and macrophage phenotype and is involved in neurodegenerative diseases (Andreasson et al., 2016).”

What the sources say

• Not checked yetcites Andreasson et al., 2016 source

In the paper

“The interaction of Aβ with RAGE causes oxidative stress in neurons, enhances inflammatory responses in microglia, and is involved in reversed transport of Aβ across the BBB in endothelial cells (Deane et al., 2012).”

What the sources say

• Not checked yetcites Deane et al., 2012 source

In the paper

“This pathway, induced in the microglial cells by anti-inflammatory cytokines, is modulated by CD33 and is down-regulated by agonists of TLR2, 4, and 9, as well as by inflammatory stimuli such as lipopolysaccharides and RNA interference. An overexpression of TREM2 promotes phagocytosis and reduces the pro-inflammatory response (Han et al., 2017).”

What the sources say

• Not checked yetcites Han et al., 2017 source

In the paper

“The signaling pathway TREM2 regulates apoptosis, the immune response, and phagocytic activity.”

In the paper

“These activated cells can release both pro- and anti-inflammatory mediators, leading to a state of chronic inflammation in the tissue.”

In the paper

“Although microglia are the main agents responsible for phagocytosis of cell debris in the CNS, the complement system can play a primordial role in removing damaged and apoptotic cells (Fakhoury, 2016).”

What the sources say

• Not checked yetcites Fakhoury, 2016 source

In the paper

“In addition, NLRP3 inflammasome activation reduces phagocytosis of Aβ by microglial cells, thus increasing the Aβ depositions and contributing to the pathogenesis of AD (Garlanda et al., 2013; Gold and El Khoury, 2015).”

What the sources say

• Not checked yetcites Garlanda et al., 2013 source
• Not checked yetcites Gold and El Khoury, 2015 source

In the paper

“After acute inflammatory damage, the brain glial cells respond to repair the tissue. If the stimulus persists, it produces an inflammatory chronic state that leads to neuronal dysfunction, injury, and loss (Streit et al., 2004; Calsolaro and Edison, 2016).”

What the sources say

• Not checked yetcites Streit et al., 2004 source
• Not checked yetcites Calsolaro and Edison, 2016 source

In the paper

“After damage, microglia transform into active phagocytes. These cells migrate to the damaged area and adopt an amoeboid morphology, releasing both pro- and anti-inflammatory molecules. They also have the capacity to remove apoptotic cells and debris.”

In the paper

“Microglial cells can activate the complement by local secretion of the complement component from both the classical and the alternative pathway and also express C3 and C5 (Luo et al., 2011).”

What the sources say

• Not checked yetcites Luo et al., 2011

In the paper

“In addition, activated microglia are capable of upregulating CD11c, MHC I, and MHC II to act as antigen-presenting cells, which activate T cells. This activation would in turn damage the nervous system (Xu et al., 2016).”

What the sources say

• Not checked yetcites Xu et al., 2016

In the paper

“Although the same JAK/STAT components are used, the gene expression in response to a specific cytokine, depending on the cell type (van Boxel-Dezaire et al., 2006).”

What the sources say

• Not checked yetcites van Boxel-Dezaire et al., 2006 source

In the paper

“Cytokines bind to receptors in the microglia and activate the JAK/STAT signaling pathway (Yan et al., 2016).”

What the sources say

• Not checked yetcites Yan et al., 2016 source

In the paper

“Microglial cells are important for the normal functioning of neurons in the CNS. They provide trophic support to neurons and regulate synapses.”

In the paper

“Both inflammation and reduced microglial phagocytic capacity in AD can contribute to the decline in synaptic plasticity observed in this pathology (Ritzel et al., 2015; Udeochu et al., 2016).”

What the sources say

• Not checked yetcites Ritzel et al., 2015 source
• Not checked yetcites Udeochu et al., 2016 source

In the paper

“The synapse loss in the hippocampus and association cortices is an early hallmark of AD and strongly correlates with cognitive impairment (Hong et al., 2016).”

What the sources say

• Not checked yetcites Hong et al., 2016 source

In the paper

“Presumably, microglial proliferation around plaques could serve as a line of defense to limit the deposition of amyloid.”

In the paper

“It has been suggested that mitochondrial malfunction leads to reduced energy metabolism and induces neuroinflammation via NO and ROS production, which ultimately entails neurodegeneration (Vivekanantham et al., 2015).”

What the sources say

• Not checked yetcites Vivekanantham et al., 2015 source

In the paper

“During development, microglia are involved in synapse elimination and these mechanisms may be aberrantly reactivated in the aged brain, contributing to the synapse loss in AD.”

In the paper

“The activation of the fractalkine receptor (CX3CR1) in microglial cells, increases synaptic strength. However, deficiency in this receptor results in a reduced hippocampal synaptic plasticity (Rogers et al., 2011; Clark et al., 2015).”

What the sources say

• Not checked yetcites Rogers et al., 2011 source
• Not checked yetcites Clark et al., 2015 source

In the paper

“TREM2 inhibits pro-inflammatory cytokine production, facilitates phagocytosis and promotes cell survival. Thus, TREM2 dysfunction could induce the loss of the homeostasis in the tissue (Painter et al., 2015).”

What the sources say

• Not checked yetcites Painter et al., 2015 source

In the paper

“In AD patients, astrocytes in the entorhinal cortex accumulate Aβ, this accumulation being positively correlated with the extent of AD (Nagele et al., 2003).”

What the sources say

• Not checked yetcites Nagele et al., 2003 source

In the paper

“In rat PD models, both deficiency CX3CL1 or CX3CR1 as well as the dysfunction of CD200-CD200R signaling have been shown to increase microglial activation and the degeneration of DA neurons (Wang et al., 2011; Zhang et al., 2011).”

What the sources say

• Not checked yetcites Wang et al., 2011 source
• Not checked yetcites Zhang et al., 2011 source

In the paper

“Moreover, astrocytes can also induce microglia to perform Aβ phagocytosis by regulating the release of the apo E and the ATP-binding cassette (ABCA) protein. Studies in vitro have demonstrated that microglial phagocytosis of Aβ is more effective in the presence of supernatants derived from astrocytes (Terwel et al., 2011).”

What the sources say

• Not checked yetcites Terwel et al., 2011 source

In the paper

“The release of brain-derived neurotrophic factor (BDNF) by microglial cells induces synaptic pruning. However, the depletion of this factor in the microglia results in learning and memory impairment (Parkhurst et al., 2013).”

What the sources say

• Not checked yetcites Parkhurst et al., 2013 source

In the paper

“Activated microglia can shed MVs in response to several signals, including cytokines. These MVs contain bioactive molecules (i.e., IL-1β, proteases, and MHC-II) which modulate the activity of neuronal and non-neuronal cells (Antonucci et al., 2012).”

What the sources say

• Not checked yetcites Antonucci et al., 2012 source

In the paper

“In addition, microglial-specific genetic alterations may be related to this microglial dysfunction. The expression of beclin 1, a protein associated with autophagy pathway, is reduced in the brain of patients with AD, leading to disruption in phagocytosis and retromer-mediated recycling of the phagocytic receptors CD36 and TREM2 in microglia (Mosher and Wyss-Coray, 2014).”

What the sources say

• Not checked yetcites Mosher and Wyss-Coray, 2014 source