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Related Concept Videos

Alzheimer's Disease: Overview01:26

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Author Spotlight: Stimulation-Based Approach to Improve Cerebral Blood Flow in Alzheimer's Model
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Cerebral blood flow decrease as an early pathological mechanism in Alzheimer's disease.

Nils Korte1, Ross Nortley1, David Attwell2

  • 1Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, UK.

Acta Neuropathologica
|September 1, 2020
PubMed
Summary
This summary is machine-generated.

Early decreases in cerebral blood flow (CBF), not amyloid beta or tau, may initiate Alzheimer's disease (AD). This review explores neglected therapeutic targets focusing on restoring CBF to combat neurodegeneration.

Keywords:
Alzheimer’sAmyloid βCapillaryCerebral blood flowNeutrophilPericyte

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Area of Science:

  • Neurology
  • Neuroscience
  • Pathophysiology

Background:

  • Current Alzheimer's disease (AD) therapies targeting amyloid beta (Aβ) and tau aggregation have shown limited success, likely due to late intervention after neuronal damage.
  • Emerging biomarkers indicate that reduced cerebral blood flow (CBF) is an early event in AD pathogenesis.

Purpose of the Study:

  • To review the role of decreased cerebral blood flow (CBF) as an initiating factor in Alzheimer's disease (AD).
  • To highlight neglected therapeutic strategies targeting early CBF reduction in AD.

Main Methods:

  • Review of existing literature on Alzheimer's disease pathogenesis, focusing on cerebral blood flow.
  • Analysis of the mechanisms linking pericyte constriction, neutrophil trapping, and clot formation to reduced CBF.
  • Examination of how reduced CBF exacerbates neurodegeneration and amyloid cascade.

Main Results:

  • Oligomeric Aβ may trigger capillary constriction by pericytes, leading to reduced CBF.
  • Reduced CBF can be further exacerbated by neutrophil trapping and clot formation.
  • Decreased CBF upregulates BACE1 and promotes tau hyperphosphorylation, amplifying AD pathology.

Conclusions:

  • Reduced cerebral blood flow (CBF) may be a critical early driver of Alzheimer's disease (AD), initiating or amplifying the amyloid cascade.
  • Novel therapeutic approaches for AD should consider targeting mechanisms that restore CBF to prevent or mitigate neurodegeneration.