Matrix metalloproteinases (MMPs) are proteolytic enzymes involved in extracellular matrix remodeling and have been implicated in Alzheimer's disease (AD) pathophysiology. This review summarizes recent research on MMPs in AD, focusing on their roles in molecular mechanisms and their potential as biomarkers or therapeutic targets. AD is a neurodegenerative disorder characterized by amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs), with genetic and environmental factors contributing to its development. The APOE ε4 allele is a significant genetic risk factor for late-onset AD (LOAD). MMPs are classified into six groups, including collagenases, gelatinases, matrilysins, stromelysins, membrane-type MMPs (MT-MMPs), and others. They regulate various physiological and pathophysiological processes, including ECM remodeling, inflammation, and BBB function. In the central nervous system (CNS), MMPs are expressed by astrocytes, microglia, and neurons, and their dysregulation is associated with AD pathology. Studies using cell cultures and human samples show that MMPs, particularly MMP-9, may influence Aβ clearance and neuroprotection. MMP-9 activity is increased in AD patients, and its levels are associated with disease progression. MMPs and their inhibitors, such as TIMPs, are also found in brain tissue and body fluids like plasma and cerebrospinal fluid (CSF). MMP-9 levels are elevated in AD patients compared to controls, and their activity is linked to cognitive decline. MMP-10 is a promising biomarker for early AD diagnosis. Sex differences in MMP/TIMP levels are observed, with higher MMP-9 levels in women. MMP activity and concentration are critical factors in AD research, and their accurate measurement is essential for understanding disease mechanisms. This review highlights the potential of MMPs as biomarkers and therapeutic targets in AD.Matrix metalloproteinases (MMPs) are proteolytic enzymes involved in extracellular matrix remodeling and have been implicated in Alzheimer's disease (AD) pathophysiology. This review summarizes recent research on MMPs in AD, focusing on their roles in molecular mechanisms and their potential as biomarkers or therapeutic targets. AD is a neurodegenerative disorder characterized by amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs), with genetic and environmental factors contributing to its development. The APOE ε4 allele is a significant genetic risk factor for late-onset AD (LOAD). MMPs are classified into six groups, including collagenases, gelatinases, matrilysins, stromelysins, membrane-type MMPs (MT-MMPs), and others. They regulate various physiological and pathophysiological processes, including ECM remodeling, inflammation, and BBB function. In the central nervous system (CNS), MMPs are expressed by astrocytes, microglia, and neurons, and their dysregulation is associated with AD pathology. Studies using cell cultures and human samples show that MMPs, particularly MMP-9, may influence Aβ clearance and neuroprotection. MMP-9 activity is increased in AD patients, and its levels are associated with disease progression. MMPs and their inhibitors, such as TIMPs, are also found in brain tissue and body fluids like plasma and cerebrospinal fluid (CSF). MMP-9 levels are elevated in AD patients compared to controls, and their activity is linked to cognitive decline. MMP-10 is a promising biomarker for early AD diagnosis. Sex differences in MMP/TIMP levels are observed, with higher MMP-9 levels in women. MMP activity and concentration are critical factors in AD research, and their accurate measurement is essential for understanding disease mechanisms. This review highlights the potential of MMPs as biomarkers and therapeutic targets in AD.