[1] 2024 Alzheimer's disease facts and figures. Alzheimers Dement, 2024; 20, 3708-821.
[2] Chen ZY, Zhang Y. Animal models of Alzheimer's disease: applications, evaluation, and perspectives. Zool Res, 2022; 43, 1026−40. doi:  10.24272/j.issn.2095-8137.2022.289
[3] Orobets KS, Karamyshev AL. Amyloid precursor protein and Alzheimer's disease. Int J Mol Sci, 2023; 24, 14794. doi:  10.3390/ijms241914794
[4] Szabo MP, Mishra S, Knupp A, et al. The role of Alzheimer's disease risk genes in endolysosomal pathways. Neurobiol Dis, 2022; 162, 105576. doi:  10.1016/j.nbd.2021.105576
[5] Rajendran K, Krishnan UM. Mechanistic insights and emerging therapeutic stratagems for Alzheimer's disease. Ageing Res Rev, 2024; 97, 102309. doi:  10.1016/j.arr.2024.102309
[6] Van Acker ZP, Bretou M, Annaert W. Endo-lysosomal dysregulations and late-onset Alzheimer's disease: impact of genetic risk factors. Mol Neurodegener, 2019; 14, 20. doi:  10.1186/s13024-019-0323-7
[7] Takasugi N, Komai M, Kaneshiro N, et al. The pursuit of the "inside" of the amyloid hypothesis-is C99 a promising therapeutic target for Alzheimer's disease? Cells, 2023; 12, 454.
[8] Zhuravleva V, Vaz-Silva J, Zhu M, et al. Rab35 and glucocorticoids regulate APP and BACE1 trafficking to modulate Aβ production. Cell Death Dis, 2021; 12, 1137. doi:  10.1038/s41419-021-04433-w
[9] Toh WH, Tan JZA, Zulkefli KL, et al. Amyloid precursor protein traffics from the Golgi directly to early endosomes in an Arl5b- and AP4-dependent pathway. Traffic, 2017; 18, 159−75. doi:  10.1111/tra.12465
[10] Mishra S, Knupp A, Szabo MP, et al. The Alzheimer's gene SORL1 is a regulator of endosomal traffic and recycling in human neurons. Cell Mol Life Sci, 2022; 79, 162. doi:  10.1007/s00018-022-04182-9
[11] Eggert S, Thomas C, Kins S, et al. Trafficking in Alzheimer's disease: modulation of APP transport and processing by the transmembrane proteins LRP1, SorLA, SorCS1c, sortilin, and calsyntenin. Mol Neurobiol, 2018; 55, 5809−29. doi:  10.1007/s12035-017-0806-x
[12] Perdigão C, Barata MA, Araújo MN, et al. Intracellular trafficking mechanisms of synaptic dysfunction in Alzheimer's disease. Front Cell Neurosci, 2020; 14, 72.
[13] Tzioras M, McGeachan RI, Durrant CS, et al. Synaptic degeneration in Alzheimer disease. Nat Rev Neurol, 2023; 19, 19−38. doi:  10.1038/s41582-022-00749-z
[14] Löscher W, Gillard M, Sands ZA, et al. Synaptic vesicle glycoprotein 2A ligands in the treatment of epilepsy and beyond. CNS Drugs, 2016; 30, 1055−77. doi:  10.1007/s40263-016-0384-x
[15] Bradberry MM, Chapman ER. All-optical monitoring of excitation-secretion coupling demonstrates that SV2A functions downstream of evoked Ca2+ entry. J Physiol, 2022; 600, 645−54. doi:  10.1113/JP282601
[16] Mecca AP, O'Dell RS, Sharp ES, et al. Synaptic density and cognitive performance in Alzheimer's disease: a PET imaging study with [11C]UCB-J. Alzheimers Dement, 2022; 18, 2527−36. doi:  10.1002/alz.12582
[17] Wu PP, Cao BR, Tian FY, et al. Development of SV2A ligands for epilepsy treatment: a review of levetiracetam, brivaracetam, and padsevonil. Neurosci Bull, 2024; 40, 594−608. doi:  10.1007/s12264-023-01138-2
[18] Tokudome K, Okumura T, Shimizu S, et al. Synaptic vesicle glycoprotein 2A (SV2A) regulates kindling epileptogenesis via GABAergic neurotransmission. Sci Rep, 2016; 6, 27420. doi:  10.1038/srep27420
[19] Mecca AP, Chen MK, O'Dell RS, et al. In vivo measurement of widespread synaptic loss in Alzheimer's disease with SV2A PET. Alzheimers Dement, 2020; 16, 974−82. doi:  10.1002/alz.12097
[20] Harper CB, Small C, Davenport EC, et al. An epilepsy-associated SV2A mutation disrupts synaptotagmin-1 expression and activity-dependent trafficking. J Neurosci, 2020; 40, 4586−95. doi:  10.1523/JNEUROSCI.0210-20.2020
[21] Lin CY, Chang MC and Jhou HJ. Effect of levetiracetam on cognition: a systematic review and meta-analysis of double-blind randomized placebo-controlled trials. CNS Drugs, 2024; 38, 1−14. doi:  10.1007/s40263-023-01058-9
[22] Knupp A, Mishra S, Martinez R, et al. Depletion of the AD risk gene SORL1 selectively impairs neuronal endosomal traffic independent of Amyloidogenic APP processing. Cell Rep, 2020; 31, 107719. doi:  10.1016/j.celrep.2020.107719
[23] Musardo S, Therin S, Pelucchi S, et al. The development of ADAM10 endocytosis inhibitors for the treatment of Alzheimer's disease. Mol Ther, 2022; 30, 2474−90. doi:  10.1016/j.ymthe.2022.03.024
[24] Hossain MI, Marcus JM, Lee JH, et al. Restoration of CTSD (cathepsin D) and lysosomal function in stroke is neuroprotective. Autophagy, 2021; 17, 1330−48. doi:  10.1080/15548627.2020.1761219
[25] Tian YL, Kang QJ, Shi XM, et al. SNX-3 mediates retromer-independent tubular endosomal recycling by opposing EEA-1-facilitated trafficking. PLoS Genet, 2021; 17, e1009607. doi:  10.1371/journal.pgen.1009607
[26] Sannerud R, Esselens C, Ejsmont P, et al. Restricted location of PSEN2/γ-secretase determines substrate specificity and generates an intracellular Aβ pool. Cell, 2016; 166, 193−208. doi:  10.1016/j.cell.2016.05.020
[27] McKendell AK, Houser MCQ, Mitchell SPC, et al. In-depth characterization of endo-lysosomal Aβ in intact neurons. Biosensors (Basel), 2022; 12, 663.
[28] Gallwitz L, Schmidt L, Marques ARA, et al. Cathepsin D: analysis of its potential role as an amyloid beta degrading protease. Neurobiol Dis, 2022; 175, 105919. doi:  10.1016/j.nbd.2022.105919
[29] Meyer H, Kravic B. The endo-lysosomal damage response. Annu Rev Biochem, 2024; 93, 367−87. doi:  10.1146/annurev-biochem-030222-102505
[30] Di YQ, Han XL, Kang XL, et al. Autophagy triggers CTSD (cathepsin D) maturation and localization inside cells to promote apoptosis. Autophagy, 2021; 17, 1170−92. doi:  10.1080/15548627.2020.1752497
[31] Prieto Huarcaya S, Drobny A, Marques ARA, et al. Recombinant pro-CTSD (cathepsin D) enhances SNCA/α-Synuclein degradation in α-Synucleinopathy models. Autophagy, 2022; 18, 1127−51. doi:  10.1080/15548627.2022.2045534
[32] Al-Kuraishy HM, Jabir MS, Al-Gareeb AI, et al. Evaluation and targeting of amyloid precursor protein (APP)/amyloid beta (Aβ) axis in amyloidogenic and non-amyloidogenic pathways: a time outside the tunnel. Ageing Res Rev, 2023; 92, 102119. doi:  10.1016/j.arr.2023.102119
[33] Eckman EA, Clausen DM, Solé-Domėnech S, et al. Nascent Aβ42 fibrillization in synaptic endosomes precedes plaque formation in a mouse model of Alzheimer's-like β-amyloidosis. J Neurosci, 2023; 43, 8812−24. doi:  10.1523/JNEUROSCI.1318-23.2023
[34] Mecca AP, Chen MK, O'Dell RS, et al. Association of entorhinal cortical tau deposition and hippocampal synaptic density in older individuals with normal cognition and early Alzheimer's disease. Neurobiol Aging, 2022; 111, 44−53. doi:  10.1016/j.neurobiolaging.2021.11.004
[35] Rossi R, Arjmand S, Bærentzen SL, et al. Synaptic Vesicle Glycoprotein 2A: features and functions. Front Neurosci, 2022; 16, 864514. doi:  10.3389/fnins.2022.864514
[36] Stout KA, Dunn AR, Hoffman C, et al. The synaptic vesicle glycoprotein 2: structure, function, and disease relevance. ACS Chem Neurosci, 2019; 10, 3927−38. doi:  10.1021/acschemneuro.9b00351
[37] Wang WY, Wang YR, Xu LM, et al. Presynaptic terminal integrity is associated with glucose metabolism in Parkinson's disease. Eur J Nucl Med Mol Imaging, 2025; 52, 1510−19. doi:  10.1007/s00259-024-06993-3
[38] Wang XL, Zhang XM, Liu J, et al. Synaptic vesicle glycoprotein 2 A in serum is an ideal biomarker for early diagnosis of Alzheimer's disease. Alzheimers Res Ther, 2024; 16, 82. doi:  10.1186/s13195-024-01440-9
[39] Fourriere L, Gleeson PA. Amyloid β production along the neuronal secretory pathway: dangerous liaisons in the Golgi? Traffic, 2021; 22, 319-27.
[40] Tan JZA, Fourriere L, Wang JQ, et al. Distinct anterograde trafficking pathways of BACE1 and amyloid precursor protein from the TGN and the regulation of amyloid-β production. Mol Biol Cell, 2020; 31, 27−44. doi:  10.1091/mbc.E19-09-0487
[41] Hur JY. γ-secretase in Alzheimer's disease. Exp Mol Med, 2022; 54, 433−46. doi:  10.1038/s12276-022-00754-8
[42] Cui YT, Zhang XM, Liu J, et al. Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease. Aging Cell, 2024; 23, e14260. doi:  10.1111/acel.14260
[43] Fourriere L, Cho EHJ, Gleeson PA. Segregation of the membrane cargoes, BACE1 and amyloid precursor protein (APP) throughout the Golgi apparatus. Traffic, 2022; 23, 158−73. doi:  10.1111/tra.12831
[44] Herman M, Randall GW, Spiegel JL, et al. Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkers. Philos Trans R Soc Lond B Biol Sci, 2024; 379, 20220387. doi:  10.1098/rstb.2022.0387
[45] Lai SSM, Ng KY, Koh RY, et al. Endosomal-lysosomal dysfunctions in Alzheimer's disease: pathogenesis and therapeutic interventions. Metab Brain Dis, 2021; 36, 1087−100. doi:  10.1007/s11011-021-00737-0
[46] Behl T, Kaur D, Sehgal A, et al. Exploring the potential role of rab5 protein in endo-lysosomal impairment in Alzheimer's disease. Biomed Pharmacother, 2022; 148, 112773. doi:  10.1016/j.biopha.2022.112773
[47] Houser MCQ, Mitchell SPC, Sinha P, et al. Endosome and lysosome membrane properties functionally link to γ-secretase in live/intact cells. Sensors (Basel), 2023; 23, 2651. doi:  10.3390/s23052651
[48] Mishra S, Jayadev S, Young JE. Differential effects of SORL1 deficiency on the endo-lysosomal network in human neurons and microglia. Philos Trans R Soc Lond B Biol Sci, 2024; 379, 20220389. doi:  10.1098/rstb.2022.0389
[49] Afghah Z, Khan N, Datta G, et al. Involvement of endolysosomes and aurora kinase A in the regulation of amyloid β protein levels in neurons. Int J Mol Sci, 2024; 25, 6200. doi:  10.3390/ijms25116200
[50] Shen Q, Wu XL, Zhang Z, et al. Gamma frequency light flicker regulates amyloid precursor protein trafficking for reducing β-amyloid load in Alzheimer's disease model. Aging Cell, 2022; 21, e13573. doi:  10.1111/acel.13573
[51] Filippone A, Praticò D. Endosome dysregulation in down syndrome: a potential contributor to Alzheimer disease pathology. Ann Neurol, 2021; 90, 4−14. doi:  10.1002/ana.26042
[52] Burrinha T, Martinsson I, Gomes R, et al. Upregulation of APP endocytosis by neuronal aging drives amyloid-dependent synapse loss. J Cell Sci, 2021; 134, jcs255752. doi:  10.1242/jcs.255752
[53] Song C, Li SF, Mai Y, et al. Dysregulated expression of miR-140 and miR-122 compromised microglial chemotaxis and led to reduced restriction of AD pathology. J Neuroinflammation, 2024; 21, 167. doi:  10.1186/s12974-024-03162-z
[54] Rao RV, Subramaniam KG, Gregory J, et al. Rationale for a multi-factorial approach for the reversal of cognitive decline in Alzheimer's disease and MCI: a review. Int J Mol Sci, 2023; 24, 1659. doi:  10.3390/ijms24021659
[55] Adepoju VA, Onyezue OI, Jamil S, et al. Lecanemab unveiled: exploring Alzheimer's treatment advancements, assessing strengths, limitations, and its therapeutic landscape position. Biomed Environ Sci, 2024; 37, 428−31.
[56] Shastri D, Raj V, Lee S. Revolutionizing Alzheimer's treatment: harnessing human serum albumin for targeted drug delivery and therapy advancements. Ageing Res Rev, 2024; 99, 102379. doi:  10.1016/j.arr.2024.102379
[57] Asiamah EA, Feng BF, Guo RY, et al. The contributions of the endolysosomal compartment and autophagy to APOEɛ4 allele-mediated increase in Alzheimer's disease risk. J Alzheimers Dis, 2024; 97, 1007−31. doi:  10.3233/JAD-230658