Elsevier

Pathology

Volume 16, Issue 3, 1984, Pages 233-234
Pathology

Etiology and pathogenesis of alzheimer's disease

https://doi.org/10.3109/00313028409068528Get rights and content

References (27)

  • G.K. Wilcock et al.

    J Neurol Sci

    (1982)
  • C.Q. Mountjoy et al.

    J Neurol Sci

    (1982)
  • W.A. Banks et al.

    Lancet

    (1983)
  • S.B. Prusiner et al.

    Cell

    (1983)
  • D.P. Perl et al.

    Science

    (1973)
  • C.L. Masters et al.

    Brain

    (1981)
  • C.L. Masters et al.

    Brain

    (1981)
  • J. Goudsmit et al.

    Neurology (NY)

    (1980)
  • H.M. Wisniewski et al.

    Ann Neurol

    (1980)
  • R.G. Struble et al.

    Science

    (1982)
  • M. Bruce et al.

    Neuropathol Appl Neurobiol

    (1975)
  • J. Tateishi et al.

    Ann Neurol

    (1984)
  • R. Sulkava et al.

    J Neurol Neurosurg Psychiatry

    (1983)
  • Cited by (5)

    • Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance

      2022, Pharmacology and Therapeutics
      Citation Excerpt :

      Electron microscopy and diffraction studies in the 1960s demonstrated that plaques and NFTs are large, organized structures of β-pleated and paired helical filaments (Eanes & Glenner, 1968; Terry, 1963; Terry, Gonatas, & Weiss, 1964). By the 1980s, multiple biochemical studies found that amyloid-beta (Aβ, 4 kDa) accumulates in these plaques as oligomers, protofibrils, and fibrillar sheets (Fig. 1A) (Glenner & Wong, 1984; Masters, 1984; Masters et al., 1985; Roher et al., 1996). Aβ is a 36-43 amino acid peptide that forms when amyloid precursor protein (APP) is cleaved by alpha- and gamma-secretases within the transmembrane region (Esch et al., 1990; Sisodia, Koo, Beyreuther, Unterbeck, & Price, 1990).

    • Display of AD Related Genes Based on GSE118553

      2021, ACM International Conference Proceeding Series
    • Etiologic theories of Alzheimer's disease

      1986, American Journal of Alzheimer's Disease and Other Dementias
    View full text