JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. British Ecological Society is collaborating with JSTOR to digitize, preserve and extend access to Journal of Animal Ecology. SUMMARY(1) Several models describing the dynamics of host-parasite associations are discussed.(2) The models contain the central assumption that the parasite increases the rate of host mortalities. The parasite induced changes in this rate are formulated as functions of the parasite numbers per host and hence of the statistical distribution of the parasites within the host population.(3) The parameters influencing the ability of the parasite to regulate the growth of its host's population, and the stability of parasite induced equilibria, are examined for each model.(4) Three specific categories of population processes are shown to be of particular significance in stabilizing the dynamical behaviour of host-parasite interactions and enhancing the regulatory role of the parasite.These categories are overdispersion of parasite numbers per host, nonlinear functional relationships between parasite burden per host and host death rate, and density dependent constraints on parasite population growth within individual hosts. INTRODUCTIONEucaryotic parasites of one kind or another play a part in the natural history of many, if not most, animals. Man is not exempt: considering helminth parasites alone, roughly 200 million people are affected by the trematode species which cause schistosomiasis and 300 million by the filarial nematode parasites. A multitude of other internal and external parasites of man produce effects ranging from minor irritations to major diseases.The relation between populations of such parasites and their hosts can be regarded as a particular manifestation of the general predator-prey interaction. Predator-prey theory has received much attention since the work of Lotka and Volterra in the 1920s, and all contemporary ecology texts give a lot of coverage to the subject. This work, however, tends to draw its inspiration, and its empirical basis, from the world of moose and wolves (with differential equations for continuously overlapping generations) or of arthropod predators and their prey (with difference equations for discrete, non-overlapping generations); see, e.g. the reviews by May (1976, ch. 4.) and Hassell (1976). That is, the extensive predator-pray literature pertains mainly to situations where (at least in effect) the predators kill and eat their prey.Analogous studies of the special kinds of predator-prey relations that are of parasito- Regulation and stability of host-parasite interactions. I Regulation and stability of host-parasite interactions. I logical interest are comparatively few. Thus relatively little is known about the effec...

The effects of selection by host immune responses on transmission dynamics was analyzed in a broad class of antigenically diverse pathogens. Strong selection can cause pathogen populations to stably segregate into discrete strains with nonoverlapping antigenic repertoires. However, over a wide range of intermediate levels of selection, strain structure is unstable, varying in a manner that is either cyclical or chaotic. These results have implications for the interpretation of longitudinal epidemiological data on strain or serotype abundance, design of surveillance strategies, and the assessment of multivalent vaccine trials.

(1) Three categories of biological processes are shown to have a destabilizing inf on the dynamical behaviour of model host-parasite associations: parasit reduction in host reproductive potential, parasite reproduction within a h directly increases parasite population size and time delays in parasite reprod transmission. (2) The importance of parasitic species as regulators of host population growth is examined in light of empirical evidence. Data from two particular laboratory studies used to indicate the magnitude of this regulatory influence. Suggestions are made concerning the type of information required from field studies to facilitate critical assessment of theoretical predictions.

CSF biomarkers, including total-tau, neurofilament light chain (NfL) and amyloid-β, are increasingly being used to define and stage Alzheimer’s disease. These biomarkers can be measured more quickly and less invasively in plasma and may provide important information for early diagnosis of Alzheimer’s disease. We used stored plasma samples and clinical data obtained from 4444 non-demented participants in the Rotterdam study at baseline (between 2002 and 2005) and during follow-up until January 2016. Plasma concentrations of total-tau, NfL, amyloid-β40 and amyloid-β42 were measured using the Simoa NF-light® and N3PA assays. Associations between biomarker plasma levels and incident all-cause and Alzheimer’s disease dementia during follow-up were assessed using Cox proportional-hazard regression models adjusted for age, sex, education, cardiovascular risk factors and APOE ε4 status. Moreover, biomarker plasma levels and rates of change over time of participants who developed Alzheimer’s disease dementia during follow-up were compared with age and sex-matched dementia-free control subjects. During up to 14 years follow-up, 549 participants developed dementia, including 374 cases with Alzheimer’s disease dementia. A log2 higher baseline amyloid-β42 plasma level was associated with a lower risk of developing all-cause or Alzheimer’s disease dementia, adjusted hazard ratio (HR) 0.61 [95% confidence interval (CI), 0.47–0.78; P < 0.0001] and 0.59 (95% CI, 0.43–0.79; P = 0.0006), respectively. Conversely, a log2 higher baseline plasma NfL level was associated with a higher risk of all-cause dementia [adjusted HR 1.59 (95% CI, 1.38–1.83); P < 0.0001] or Alzheimer’s disease [adjusted HR 1.50 (95% CI, 1.26–1.78); P < 0.0001]. Combining the lowest quartile group of amyloid-β42 with the highest of NfL resulted in a stronger association with all-cause dementia [adjusted HR 9.5 (95% CI, 2.3–40.4); P < 0.002] and with Alzheimer’s disease [adjusted HR 15.7 (95% CI, 2.1–117.4); P < 0.0001], compared to the highest quartile group of amyloid-β42 and lowest of NfL. Total-tau and amyloid-β40 levels were not associated with all-cause or Alzheimer’s disease dementia risk. Trajectory analyses of biomarkers revealed that mean NfL plasma levels increased 3.4 times faster in participants who developed Alzheimer’s disease compared to those who remained dementia-free (P < 0.0001), plasma values for cases diverged from controls 9.6 years before Alzheimer’s disease diagnosis. Amyloid-β42 levels began to decrease in Alzheimer’s disease cases a few years before diagnosis, although the decline did not reach significance compared to dementia-free participants. In conclusion, our study shows that low amyloid-β42 and high NfL plasma levels are each independently and in combination strongly associated with risk of all-cause and Alzheimer’s disease dementia. These data indicate that plasma NfL and amyloid-β42 levels can be used to assess the risk of developing dementia in a non-demented population. Plasma NfL levels, although not specific, may also be useful in monitoring progression of Alzheimer’s disease dementia.