SummaryBaseline studies of 111indium oxine labelled platelet life-span, platelet α-granule release products, β-thromboglobulin (βTG) and platelet factor 4 (PF4), and factor VIII related activities were performed on 9 asymptomatic patients with sickle cell disease, who were subsequently randomised in a prospective double-blind trial of ticlopidine (250 mg. b. d.) or placebo for one month and the investigations repeated. Control studies indicated that 5 of the 9 patients had shortened platelet survivals: mean βTG (50.8 ng/ ml) and PF4 (19.5 ng/ml), factor VIII: C (283.4 i. u./dl) and factor VIIIR: AG (168.7 u/dl) levels were raised. Ticlopidine treatment did not significantly improve platelet life-span or factor VIII levels, though it was associated with reduced values of βTG and PF4. One patient taking ticlopidine developed an infarctive sickle crisis. Although ticlopidine blocked platelet activation, this alone did not improve platelet survival or prevent sickle crisis: in view of evidence of platelet activation in sickle cell disease, however, a longer trial of prophylactic antiplatelet drugs might be warranted.

Previous studies have established cross-cultural methods to screen for ageing-related dementia and susceptibility genes, in particular Alzheimer's disease (AD) among the Canadian Cree, African Americans and Yoruba in Nigeria. We determined whether the Community Screening Interview for Dementia (CSID), translated into Kikuyu, a major language of Kenya, could be used to evaluate dementia of the Alzheimer type. Using two sets of coefficients of cognitive and informant scores, two discriminant function (DF) scores were calculated for each of 100 elderly (>65 years) Nyeri Kenyans. When the cut-off points were selected for 100% sensitivities, the specificities of the DF scores were remarkably similar (93.75%) in the Kenyan sample. We propose the adapted CSID can be utilised to detect dementia among East Africans. We also show that apolipoprotein E ε4 allele frequencies were high (∼30%) and not different between normal subjects and those with probable AD. There was no evidence to suggest years of education or vascular factors were associated with dementia status.

Khat products and chewing practices are common in East Africa, Middle East for centuries with concomitant socio-economic and public health repercussions. We assessed memory deficits associated with khat use in rodents. Young male CBA mice, 5-7 weeks old (n = 20), weighing 25-35 g were used. Mice were treated with either 40, 120 or 360 mg/kg body weight (bw) methanolic khat extract, or 0.5 ml saline for 10 days. Spatial acquisition, reversal and reference memory were assessed using modified Morris Water maze (MMWM). Mice treated with 40 mg/kg khat extract had longer (t4 = 4.12 p = 0.015) and t4 = 2.28 p = 0.065) escape latency on first and second day during reversal relative to the baseline. Under 120 mg/kg khat dose, the escape latency was shorter (t4 = -2.49 p = 0.05) vs (t3 = -2.5 p = 0.05) on third and fourth day. Further, treatment with 360 mg/kg khat extract resulted in significantly longer time (49.13, 33.5, 40.2 and 35.75) vs. (23.5 s), compared to baseline. Mice treated with khat or control preferred the target quadrant post acquisition while differential pattern was seen during reversal phase. Mice treated with 40 or 120 mg/kg khat showed significant preference for target quadrant. Substantial time (19.9) was spent in the old target compared to the new (16.9 s) by animals treated with highest dose however, the difference was not significant. There is a biological plausibility that chronic khat use may induce memory deficits and impair cognitive flexibility. The differential patterns of memory deficits may reflect the differences in dose effect as well as time dependent impairment.

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