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Advanced Neurology Graphene quantum dots approach in AD

Figure 1. Synthesis of GQDs. Image created by the authors using Canva and Microsoft word.
Abbreviations: GO: Graphene oxide; GQD: Graphene quantum dot; HNO : Nitric acid; H SO : Sulfuric acid; KMnO : Potassium permanganate;
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4
4
3
KOH: Potassium hydroxide; NaOH: Sodium hydroxide; PAH: Polycyclic aromatic hydrocarbon.
AD is characterized by extracellular amyloid plaques
composed of aggregated Aβ and intracellular NFTs,
primarily formed from hyperphosphorylated tau protein. Over-production or Formation of Aβ
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Amyloid deposits, as illustrated in Figure 2, accumulate impaired clearance oligomers and Neurotoxicity
first in the hippocampus and basal regions, gradually of Aβ aggregates
recruiting additional Aβ peptides and contributing to
increased aggregation, mitochondrial dysfunction, and
synaptic impairment. This subsequently activates microglia Figure 2. The cascade begins with the overproduction or impaired
and astrocytes, triggering inflammatory and oxidative clearance of Aβ, eventually leading to the formation of oligomers and
processes that eventually lead to widespread neuronal aggregates, which contribute to neurotoxicity. Image created by the
dysfunction and apoptosis. The progression of AD involves authors using Microsoft Word.
Abbreviation: Aβ: Amyloid-beta.
Aβ plaque deposition extending from the hippocampus to
cortical regions, including the amygdala, diencephalon, and 5. Cobalamin deficiency
basal ganglia. This deposition occasionally reaches severe
stages in the cerebellar and lower brainstem regions. This Vitamin B12 deficiency is implicated as a risk factor for AD
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advanced deposition facilitates tau aggregation, notably in due to its role as a cofactor for methionine synthase, crucial
the entorhinal and locus coeruleus regions, extending into for converting homocysteine to methionine. Deficiency
the hippocampus and cortical areas. 51 of vitamin B12 leads to hyperhomocysteinemia, which is

Volume 4 Issue 4 (2025) 21 doi: 10.36922/an.7087