The impact of apolipoprotein E (ApoE) isoforms on sporadic Alzheimer's disease has long been studied; however, the influences of apolipoprotein E gene (APOE) on healthy and pathological human brains are not fully understood. ApoE exists as three common isoforms (ApoE2, ApoE3, and ApoE4), which differ in two amino acid residues. Traditionally, ApoE binds cholesterol and phospholipids and ApoE isoforms display different affinities for their receptors, lipids transport and distribution in the brain and periphery. The role of ApoE in the human depends on ApoE isoforms, brain regions, aging, and neural injury. APOE ε4 is the strongest genetic risk factor for sporadic Alzheimer's disease, considering its role in influencing amyloid-beta metabolism. The exact mechanisms by which APOE gene variants may increase or decrease Alzheimer's disease risk are not fully understood, but APOE was also known to affect directly and indirectly tau-mediated neurodegeneration, lipids metabolism, neurovascular unit, and microglial function. Consistent with the biological function of ApoE, ApoE4 isoform significantly altered signaling pathways associated with cholesterol homeostasis, transport, and myelination. Also, the rare protective APOE variants confirm that ApoE plays an important role in Alzheimer's disease pathogenesis. The objectives of the present mini-review were to describe classical and new roles of various ApoE isoforms in Alzheimer's disease pathophysiology beyond the deposition of amyloid-beta and to establish a functional link between APOE, brain function, and memory, from a molecular to a clinical level. APOE genotype also exerted a heterogeneous effect on clinical Alzheimer's disease phenotype and its outcomes. Not only in learning and memory but also in neuropsychiatric symptoms that occur in a premorbid condition. Clarifying the relationships between Alzheimer's disease-related pathology with neuropsychiatric symptoms, particularly suicidal ideation in Alzheimer's disease patients, may be useful for elucidating also the underlying pathophysiological process and its prognosis. Also, the effects of anti-amyloid-beta drugs, recently approved for the treatment of Alzheimer's disease, could be influenced by the APOE genotype.
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http://dx.doi.org/10.4103/1673-5374.375316 | DOI Listing |
Adv Sci (Weinh)
January 2025
School of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
β-secretase (BACE1) is instrumental in amyloid-β (Aβ) production, with overexpression noted in Alzheimer's disease (AD) neuropathology. The interaction of Aβ with the receptor for advanced glycation endproducts (RAGE) facilitates cerebral uptake of Aβ and exacerbates its neurotoxicity and neuroinflammation, further augmenting BACE1 expression. Given the limitations of previous BACE1 inhibition efforts, the study explores reducing BACE1 expression to mitigate AD pathology.
View Article and Find Full Text PDFActa Neuropathol Commun
January 2025
Department of Biological Sciences, Purdue University, 915 Mitch Daniels Blvd, West Lafayette, IN, USA.
Dementia refers to an umbrella phenotype of many different underlying pathologies with Alzheimer's disease (AD) being the most common type. Neuropathological examination remains the gold standard for accurate AD diagnosis, however, most that we know about AD genetics is based on Genome-Wide Association Studies (GWAS) of clinically defined AD. Such studies have identified multiple AD susceptibility variants with a significant portion of the heritability unexplained and highlighting the phenotypic and genetic heterogeneity of the clinically defined entity.
View Article and Find Full Text PDFNeurotherapeutics
January 2025
Department of Biochemistry, University of Alberta, Edmonton, Alberta, T6G 2H7, Canada. Electronic address:
Amyloidogenic protein aggregation is a pathological hallmark of Alzheimer's Disease (AD). As such, this critical feature of the disease has been instrumental in guiding research on the mechanistic basis of disease, diagnostic biomarkers and preventative and therapeutic treatments. Here we review identified molecular triggers and modulators of aggregation for two of the proteins associated with AD: amyloid beta and tau.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
First Operating Room, The First Hospital of Jilin University, Changchun, China. Electronic address:
Background: Certain peripheral proteins are believed to be involved in the development of Alzheimer's disease (AD), but the roles of other new protein biomarkers are still unclear. Current treatments aim to manage symptoms, but they are not effective in stopping the progression of the disease. New drug targets are needed to prevent Alzheimer's disease.
View Article and Find Full Text PDFNeuroscience
January 2025
Departamento de Genómica, Instituto de Investigaciones Biológicas Clemente Estable, MEC, Av. Italia 3318, Montevideo, CP 11600, Uruguay; Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Iguá, Montevideo, 4225, CP 11400, Uruguay. Electronic address:
Local protein synthesis (LPS) in axons is now recognized as a physiological process, participating both in the maintenance of axonal function and diverse plastic phenomena. In the last decades of the 20th century, the existence and function of axonal LPS were topics of significant debate. Very early, axonal LPS was thought not to occur at all and was later accepted to play roles only during development or in response to specific conditions.
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