Cerebral Amyloid β Protein Deposits and Other Alzheimer Lesions in Non‐Demented Elderly East Africans

Abstract

There is little knowledge of the existence of Alzheimer disease (AD) or Alzheimer type of dementia in indigenous populations of developing countries. In an effort to evaluate this, we assessed the deposition of amyloid beta (A beta) protein and other lesions associated with AD in brains of elderly East Africans. Brain tissues were examined from 32 subjects, aged 45 to 83 years with no apparent neurological disease, who came to autopsy at two medical Institutions in Nairobi and Dar es Salaam. An age-matched sample from subjects who had died from similar causes in Cleveland was assessed in parallel. Of the 20 samples from Nairobi, 3 (15%) brains exhibited neocortical A beta deposits that varied from numerous diffuse to highly localized compact or neuritic plaques, many of which were also thioflavin S positive. Two of the cases had profound A beta deposition in the prefrontal and temporal cortices and one of these also exhibited moderate to severe cerebral amyloid angiopathy. Similarly, 2 of the 12 samples from Dar es Salaam exhibited diffuse and compact A beta deposits that were also predominantly reactive for the longer A beta 42 species compared to A beta 40. We also noted that A beta plaques were variably immunoreactive for amyloid associated proteins, apolipoprotein E, serum amyloid P and complement C3. Tau protein reactive neurofibrillary tangles (NFT) were also evident in the hippocampus of 4 subjects. By comparison, 4 (20%) of the 20 samples from randomly selected autopsies performed in Cleveland showed A beta deposits within diffuse and compact parenchymal plaques and the vasculature. These observations suggest A beta deposition and some NFT in brains of non-demented East Africans are qualitatively and quantitatively similar to that in age-matched elderly controls from Cleveland. While our small scale study does not document similar prevalence rates of preclinical AD, it suggests that elderly East Africans are unlikely to escape AD as it is known in developed countries.

Epidemiology of neurodegenerative diseases in sub-Saharan Africa: a systematic review

“…The overall study size varied from 56 to 2494 in community-based studies and from 23 to 240,294 in hospital-based investigations. The prevalence of dementia ranged from <1% to 10.1% in population-based studies [32,34-57] and from <1% to 47.8% in hospital-based studies [16,21,30,33,38,58-69]. …”

Profiles of Alzheimer's Disease-Related Pathology in an Aging Urban Population Sample in India

“…To date, there have been several case reports of neuropathologically-confirmed cases of AD and four studies on pathology of AD from India [25–29] and other LMICs [30–33]. One of these studies reported a total absence of AD-pathology [32] and another reported only 6% of the cases with SP and 88% showing NFT [28].…”

“…One of these studies reported a total absence of AD-pathology [32] and another reported only 6% of the cases with SP and 88% showing NFT [28]. A smaller study (32 cases) from East Africa [33] showed diffuse or dense amyloid deposits and NFT comparable to age-matched cases from Cleveland, USA. Yasha and colleagues [29] in a study on AD-pathology in 53 autopsy-derived cases collected over 10 years in Bangalore, India, suggested that the AD related lesions were similar to that reported in the HIC, although they did not conduct a direct comparison.…”

Specific Mechanism for Blood Inflow Stimulation in Brain Area Prone to Alzheimer’s Disease Lesions

“…Abetas concentrations in CSF are increased in healthy humans over 59 years of age (Shoji et al, 2001), and just during aging in the brain of neurologically intact humans Abetas in monomeric, oligomeric, and aggregated forms appear. Of significance, increased amyloid quantities are found exactly in the AHBC area (Tomlinson et al, 1968;Dayan, 1970;Ulrich, 1982;Averback, 1983;Miller et al, 1984;Ulrich, 1985;Mann et al, 1987;Crystal et al, 1988;Mann et al, 1990;Arriagada et al, 1992b;Dickson et al, 1992;Bouras et al, 1994;Morys et al, 1994;Vermersch et al, 1995;Ogeng'o et al, 1996;Yasha et al, 1997;Davis et al, 1999;Miyakawa et al, 2000;Schmitt et al, 2000), which, in all likelihood, is the most suitable (if not the sole) place for intensive formation of these peptides.…”