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Despite extensive research, disease-modifying treatments remain elusive, with current management primarily focusing on symptom control

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doi: 10.2174/1389557516666151120115027

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Impairments in the supply of GTP could influence the age-related net production and clearance of amyloid (A42 and A45) resulting in accumulation of early endosomes containing Rab5 on their surface, Rab7decorated late endosomes, and p62 associated autophagosomes, as we have seen in neurons from old AD mice [1]