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Despite the consensus among seniors and primary care physicians on the importance of short cognitive assessments for dementia detection, only half of seniors have been assessed, with just 16 percent undergoing regular evaluations. Educational initiatives are available to increase the use of these assessments in primary care, according to Alzheimer's Association surveys.Alzheimer's disease (AD) pathogenesis involves oxidative stress/mitochondrial dysfunction, amyloid/tau toxicity, and cholinergic dysfunction. Among the therapeutic targets, Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is crucial due to its role in the amyloidogenic cleavage of APP, generating Amyloid ? (A?). BACE1, a ?-secretase, also cleaves substrates like neuregulin and the ?2 subunit of the voltage-gated sodium channel, essential for brain development and function. BACE1 is modulated post-translationally by factors linked to both physiological and pathological functions. However, developing small molecule inhibitors for BACE1 has posed challenges for AD treatment.
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Despite the consensus among seniors and primary care physicians on the importance of short cognitive assessments for dementia detection, only half of seniors have been assessed, with just 16 percent undergoing regular evaluations. Educational initiatives are available to increase the use of these assessments in primary care, according to Alzheimer's Association surveys.Alzheimer's disease (AD) pathogenesis involves oxidative stress/mitochondrial dysfunction, amyloid/tau toxicity, and cholinergic dysfunction. Among the therapeutic targets, Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is crucial due to its role in the amyloidogenic cleavage of APP, generating Amyloid ? (A?). BACE1, a ?-secretase, also cleaves substrates like neuregulin and the ?2 subunit of the voltage-gated sodium channel, essential for brain development and function. BACE1 is modulated post-translationally by factors linked to both physiological and pathological functions. However, developing small molecule inhibitors for BACE1 has posed challenges for AD treatment.