We are analyzing https://link.springer.com/article/10.1007/s00401-009-0498-z.

Title:
Microvasculature changes and cerebral amyloid angiopathy in Alzheimer’s disease and their potential impact on therapy | Acta Neuropathologica
Description:
The introduction of immunotherapy and its ultimate success will require re-evaluation of the pathogenesis of Alzheimer’s disease particularly with regard to the role of the ageing microvasculature and the effects of APOE genotype. Arteries in the brain have two major functions (a) delivery of blood and (b) elimination of interstitial fluid and solutes, including amyloid-β (Aβ), along perivascular pathways (lymphatic drainage). Both these functions fail with age and particularly severely in Alzheimer’s disease and vascular dementia. Accumulation of Aβ as plaques in brain parenchyma and artery walls as cerebral amyloid angiopathy (CAA) is associated with failure of perivascular elimination of Aβ from the brain in the elderly and in Alzheimer’s disease. High levels of soluble Aβ in the brain correlate with cognitive decline in Alzheimer’s disease and reflect the failure of perivascular drainage of solutes from the brain and loss of homeostasis of the neuronal environment. Clinically and pathologically, there is a spectrum of disease related to functional failure of the ageing microvasculature with “pure” Alzheimer’s disease at one end of the spectrum and vascular dementia at the other end. Changes in the cerebral microvasculature with age have a potential impact on therapy with cholinesterase inhibitors and especially on immunotherapy that removes Aβ from plaques in the brain, but results in an increase in severity of CAA and no clear improvement in cognition. Drainage of Aβ along perivascular pathways in ageing artery walls may need to be improved to maximise the potential for improvement of cognitive function with immunotherapy.
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google, scholar, pubmed, cas, article, disease, alzheimers, amyloid, brain, cerebral, weller, neuropathol, angiopathy, neurol, alzheimer, abeta, pathology, human, nicoll, perivascular, acta, pathol, doijx, vascular, dementia, dois, love, roher, exp, fluid, drainage, appl, neurobiol, doi, kuo, amyloidbeta, boche, peptide, beta, research, immunotherapy, pathogenesis, blood, pathways, cognitive, betaamyloid, perry, cortical, beach, deposition,

Topics {✒️}

month download article/chapter age-related beta-amyloid deposition amyloid-beta attenuates alzheimer-disease pro-caa position statement age-related microvascular degeneration cerebral beta-amyloid angiopathy ldl receptor-related protein-1 cerebral beta-amyloid angiopathies amyloid-beta peptide remnants beta-amyloid core protein full article pdf potential disease-modifying agents betapp transgenic mice medical research council privacy choices/manage cookies cerebral microvascular alterations cerebral amyloid angiopathy including amyloid-β increased vascular amyloid cerebral amyloid angiopathies beta amyloid deposition leptomeningeal cerebrovascular amyloid neurodegenerative disorders arterial amyloid angiopathy vascular cognitive impairment white matter damage white matter lesions amyloid beta-peptide amyloid-beta peptide amyloid beta accumulates amyloid-beta peptides beta-amyloid formation alzheimer research trust transgenic mouse models imaging–pathological correlations cserr hf cerebral blood vessels de jong gi selkoe dj post-mortem correlates central nervous system white matter pathology blood–brain barrier blood-brain barrier beta-amyloid pathology chronic hypoperfusion injury prion disorders article weller cortical blood vessels intracranial blood vessels

Questions {❓}

Bechmann I, Galea I, Perry VH (2007) What is the blood–brain barrier (not)?
Bedford L, Hay D, Paine S, Rezvani N, Mee M, Lowe J, Mayer RJ (2008) Is malfunction of the ubiquitin proteasome system the primary cause of alpha-synucleinopathies and other chronic human neurodegenerative disease?
Hatterer E, Davoust N, Didier-Bazes M, Vuaillat C, Malcus C, Belin MF, Nataf S (2006) How to drain without lymphatics?

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