Alzheimer’s Disease

Alzheimer’s Disease — Neurodegeneration up Close

From amyloid biochemistry and tau pathology to lecanemab and prevention — eight integrating modules.

Why a course on Alzheimer’s?

Alzheimer’s disease (AD) accounts for roughly two-thirds of the ~55 million people living with dementiaworldwide; that number is projected to triple by 2050. AD is the 7th-leading cause of death globally and the most expensive disease per patient-yearin many high-income countries due to long-term care.

Despite a century of work since Alois Alzheimer’s 1906 case report on Auguste Deter, the disease has only recently entered the era of disease-modifying therapy. The 2023 approval of lecanemab and 2024 approval of donanemab — both anti-amyloid monoclonals — marked the first interventions that meaningfully slow clinical progression. The course traces the biology, the diagnostic revolution of biomarkers, and the open frontier of tau- and inflammation-targeted therapy. It cross-references Neuroscience, Cell Physiology, Pharmacology, and Stroke.

Course Parts

Part I

Overview & Epidemiology

Definitions, dementia spectrum, ~55 M people with dementia globally, ~70% of which is AD; demographic projections, the cost of care, the disease as the largest neurological burden of the coming decades.

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Part II

Neuroanatomy of AD

Entorhinal cortex → hippocampus → temporoparietal → frontal: the canonical Braak staging trajectory. The default-mode network. Why memory is hit first.

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Part III

Amyloid Cascade

Aβ peptide generation: APP processing, β- and γ-secretase, Aβ42:Aβ40 ratio, oligomers vs plaques, the Hardy-Selkoe hypothesis and its 30-year evolution.

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Part IV

Tau & Tauopathy

Tau hyperphosphorylation, paired helical filaments, neurofibrillary tangles. Why tau correlates better with cognitive decline than amyloid.

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Part V

Genetics & Risk Factors

Autosomal-dominant familial AD (APP, PSEN1, PSEN2). The APOE-ε4 allele — risk and dose response. TREM2, CR1, CLU, and the genome-wide picture.

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Part VI

Diagnosis & Biomarkers

Clinical criteria (NIA-AA 2018, ATN), CSF Aβ42/p-tau, amyloid PET (PiB, florbetapir), tau PET, blood biomarkers (p-tau217), volumetric MRI.

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Part VII

Therapy

Cholinesterase inhibitors, memantine, anti-amyloid monoclonals (aducanumab, lecanemab, donanemab) and the ARIA-E/H controversy, anti-tau therapy in development.

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Part VIII

Prevention & Future

Lifestyle (FINGER trial), midlife BP/diabetes, the SPRINT-MIND result, sleep & glymphatic clearance, exercise, cognitive reserve. Drug pipelines beyond amyloid.

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What you’ll learn

  • Distinguish AD clinically from other dementias (LBD, FTD, vascular, mixed).
  • Trace APP processing through α-, β-, and γ-secretase to Aβ peptides.
  • Reason about why oligomers, not plaques, may be the toxic species.
  • Predict APOE-ε4 dose effect on lifetime risk.
  • Read CSF and amyloid-PET biomarker reports under the ATN framework.
  • Anticipate ARIA-E/H risk in patients on anti-amyloid antibodies.
  • Counsel a patient on the FINGER lifestyle bundle.
  • Critically evaluate the amyloid hypothesis after 30 years.

Prerequisites

Working knowledge of CNS anatomy, basic biochemistry of proteostasis, and membrane-protein processing. The course cross-references Neuroscience, Cell Physiology, and Biochemistry.

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