{"id":23033,"date":"2026-08-07T12:52:20","date_gmt":"2026-08-07T10:52:20","guid":{"rendered":"https:\/\/www.biolife-publisher.it\/ejnd\/?p=23033"},"modified":"2026-08-07T13:08:49","modified_gmt":"2026-08-07T11:08:49","slug":"amyloid-beta-activates-microglia-in-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/www.biolife-publisher.it\/ejnd\/2026\/08\/07\/amyloid-beta-activates-microglia-in-alzheimers-disease\/","title":{"rendered":"AMYLOID BETA ACTIVATES MICROGLIA IN ALZHEIMER’S DISEASE"},"content":{"rendered":"

M. Mattoscio1* <\/sup>and C. Cuccurullo2<\/sup><\/p>\n

1 <\/sup>Imperial College Healthcare NHS Trust, Romford, United Kingdom;
\n2 <\/sup>Department of Medicine and Ageing Sciences, University \u201cGabriele d\u2019Annunzio\u201d of Chieti\u2010Pescara, Chieti, Italy.<\/p>\n

*Correspondence to<\/em>:
\nMiriam Mattoscio,
\nImperial College Healthcare NHS Trust,
\nRomford, United Kingdom.
\ne-mail: m.mattoscio@imperial.ac.uk<\/p>\n\n\n\n
Received: 13 May, 2026
\nAccepted: 07 August, 2026
\n\"adobe-pdf-download-icon\"<\/a><\/td>\n		ISSN 2279-5855 print \/ 3103-7364 [online]
\nCopyright 2026 \u00a9 by Biolife Publisher
\nThis publication and\/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

ABSTRACT<\/strong><\/p>\n

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of extracellular amyloid-\u03b2 plaques and hyperphosphorylated tau neurofibrillary tangles, leading to neuronal dysfunction, cognitive decline, and loss of daily functioning. Microglia are the resident immune cells of the central nervous system (CNS) that maintain neuronal homeostasis through phagocytosis, synaptic remodelling, and neurotrophic support while responding to pathogens and tissue damage via pattern-recognition receptors. In AD, amyloid-\u03b2 activates microglia, promoting a shift toward a pro-inflammatory phenotype that contributes to neuroinflammation and neuronal injury. Microglia respond to amyloid-\u03b2 accumulation in AD, where their balance between pro-inflammatory and anti-inflammatory functions influences neuroinflammation, amyloid clearance, and disease progression.<\/p>\n

KEYWORDS:<\/strong> Alzheimer\u2019s Disease, CNS, microglia, neurodegenerative disease, amyloid beta<\/em><\/p>\n

\u00a0<\/strong><\/p>\n

INTRODUCTION<\/strong><\/p>\n

 <\/p>\n

Alzheimer’s disease (AD) is is a progressive neurodegenerative disease that is the most common cause of deficits in memory, language, behavior, and other cognitive functions globally (1). AD is due in part to aging and the individual losing the ability to perform essential daily activities (2). The deposition of amyloid-\u03b2 plaques and neurofibrillary tangles of hyperphosphorylated tau protein characterizes the disease (3).\u00a0 The neurodegenerative process of AD requires timely diagnosis and a multidisciplinary approach (4).\u00a0Biomarkers in brain fluid, diagnostic imaging, brain autopsy, and anti-amyloid-\u03b2 antibody testing, are useful for diagnosis (5). The prevalence of AD continues to grow, resulting in burdens on society and the healthcare system (6).<\/p>\n

In AD, amyloid plaques, protein fragments normally produced by the brain, can accumulate between neurons (7). Amyloid-\u03b2 plaques in AD are extracellular accumulations composed primarily of amyloid-\u03b2 peptides but also contain many other cellular and molecular elements (8). In chronic disease, amyloid-\u03b2 increases and microglia become activated and recognize amyloid-\u03b2 aggregates (9). Plaques can impair communication between neurons, contribute to synapse loss, decline in memory and cognitive functions, and generate inflammation (2).<\/p>\n

 <\/p>\n

MICROGLIA AND ALZHEIMER’S DISEASE<\/strong><\/p>\n

 <\/p>\n

The accumulation of amyloid-\u03b2 plaques and neurofibrillary tangles of hyperphosphorylated tau protein characterizes neurodegeneration in AD (10). Amyloid-\u03b2 is a short-chain peptide derived from the breakdown of a protein called amyloid precursor protein (APP) (11).\u00a0 This protein is normally present in nerve cell membranes, and under physiological conditions, amyloid-\u03b2 is normally produced and then eliminated from the body (12). In AD, amyloid-\u03b2 accumulates because it is either overproduced or not eliminated effectively (13).<\/p>\n

The advent of the first anti-amyloid antibodies for the treatment of AD was a major milestone in the clinical management of this condition (14). Anti-amyloid antibodies aim to slow the progression of AD in its early stages, while previously, therapy focused primarily on alleviating symptoms (15,16). Unlike traditional therapies, which primarily relieve symptoms, these drugs target the disease by removing amyloid-\u03b2 aggregates from the brain (15).\u00a0Lecanemab is used to confirm the presence of cerebral amyloid and other drugs are used to treat mild AD and non-severe cognitive impairment (17). Some of these include donanemab, which acts on a modified form of the amyloid-\u03b2 protein and slows the progression of the disease, especially in patients treated in the very early stages, and aducanumab, whose effectiveness is controversial and therefore limited in use (18). These antibodies bind to amyloid-\u03b2 plaques in the brain and promote their elimination by the immune system. The goal is to slow neuronal damage, not reverse what has already occurred. Treatment with these antibodies causes side effects such as amyloid-related imaging abnormalities (ARIA), which include hemorrhages and cerebral edema (17).\u00a0 Although these therapies are important for therapy, they only slow the disease; they do not rebuild neurons and do not lead to a cure (19).<\/p>\n

Microglia cells reside in the central nervous system (CNS) and arise from myeloid precursors in the yolk sac during embryonic development (20). Microglia are true sentinels of the brain parenchyma and are responsible for phagocytosis of cellular debris, apoptotic cells, and microorganisms (21,22).\u00a0They maintain neuronal homeostasis, remodel synaptic connections, and produce neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) (23).<\/p>\n

Viruses, bacteria, and other microorganisms activate microglia through signal recognition receptors such as pattern recognition receptors (PRRs), Toll-like receptors (TLR)2 and TLR4, CD36, RAGE, and NOD-like receptors (24).\u00a0 These receptors recognize damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), inducing cell migration, proliferation, phagocytosis, and the secretion of inflammatory mediators (25).<\/p>\n

In AD, microglia play an important role in protection, neuroinflammation and disease progression (26). Like macrophages, microglia are also divided into two phenotypes: M1 pro-inflammatory and M2 specialized in the resolution of inflammation and tissue repair, effects that can also present intermediate functional states (27). M1 cells of microglia are stimulated by various inflammatory proteins such as lipopolysaccharide (LPS), interferon-gamma (IFN-\u03b3), and amyloid-\u03b2, which lead to the production of IL-1\u03b2, IL-6, TNF, nitric oxide (NO), and reactive oxygen species (ROS) (28). These compounds cause neurotoxicity, oxidative stress, and neuronal death (29). Anti-inflammatory M2 cells are stimulated by IL-10, IL-4, and IL-13 and produce neurotrophic factors, IL-10, transforming growth factor beta (TGF-\u03b2), and arginase-1, which cause tissue repair, increased amyloid phagocytosis, and resolution of inflammation (30).<\/p>\n

In AD, amyloid-\u03b2 plaques activate several microglial receptors, such as TLR2\/4, RAGE, TREM2, and CD36, resulting in initial phagocytosis of amyloid-\u03b2, production of ROS, inflammasome activation, and production of pro-inflammatory cytokines (31). In the early stages of the disease, the immune response is protective, while in the chronic stages it becomes damaging (Fig.1).<\/p>\n

 <\/p>\n

\"\"<\/p>\n

Fig. 1.<\/strong> The deposition of amyloid-\u03b2 in the brain is one of the initial events of Alzheimer’s disease (AD). This induces microglial activation, resulting in the production of inflammatory cytokines that contribute to the progression of neurodegeneration.<\/em><\/p>\n

 <\/p>\n

Inflammatory cytokines induced by amyloid-\u03b2 plaques activate NLR family pyrin domain containing 3 (NLRP3), which in turn activates caspase-1, resulting in the maturation of inflammatory IL-1\u03b2 and IL-18 (32).\u00a0 Additionally, activated microglia produce ROS through NADPH oxidase (NOX2) and generate superoxide, hydrogen peroxide, and NO (33). NO reacts with superoxide to form peroxynitrite, which causes DNA damage, mitochondrial damage, lipid damage, and protein damage (34).<\/p>\n

Triggering receptor expressed on myeloid cells 2 (TREM2) is a key gene associated with the genetic risk of AD (35). It increases microglial survival, promotes phagocytosis, facilitates amyloid-\u03b2 clearance, and limits the inflammatory response; these effects are reduced in TREM2 genetic mutations (36).<\/p>\n

The most important gene risk factor for AD is the APOE \u03b54 allele, which influences the immune response, microglial activity, and lipid metabolism. Individuals carrying APOE \u03b54 have decreased amyloid-\u03b2 clearance and increased neurodegeneration and inflammation (37). Furthermore, microglia also contribute to the spread of Tau pathology, with the risk of neuronal kinase activation, release of Tau-containing exosomes, cytokine release, and neuroinflammation (38).<\/p>\n

 <\/p>\n

CONCLUSIONS<\/strong><\/p>\n

 <\/p>\n

In AD, microglia initially play a protective role. However, as the disease progresses, their activation becomes chronic and pathological, with the release of pro-inflammatory cytokines, ROS, and activation of the NLRP3 inflammasome. These fuel neuroinflammation, promoting synaptic loss and accelerating neurodegeneration to contribute to the development of dementia.<\/p>\n

 <\/p>\n

Conflict of interest <\/em><\/p>\n

The authors declare that they have no conflict of interest.<\/p>\n

 <\/p>\n

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