Abstract:
:There is no unifying hypothesis to account for the anatomical distribution of neuropathology, the involvement of beta-amyloid precursor protein (beta APP) and the role of increasing age in triggering the Alzheimer disease process. We report here that layer II pre-alpha neurones in transentorhinal and entorhinal cortex contain more beta APP immunoreactivity than other cortical neurones in normal individuals. This immunoreactivity increased in the early stages of Alzheimer's disease and was lost as the disease progressed. These neurones are known to undergo genetically programmed re-sprouting and synaptogenesis during the fifth and sixth decades of life. We hypothesize that these phenomena are related and that the Alzheimer's disease process originates in entorhinal cortex neurones due to the enhancement of their normally high content of beta APP during age-related resprouting.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Roberts GW,Nash M,Ince PG,Royston MC,Gentleman SMdoi
10.1097/00001756-199301000-00001subject
Has Abstractpub_date
1993-01-01 00:00:00pages
7-9issue
1eissn
0959-4965issn
1473-558Xjournal_volume
4pub_type
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