Intruder Model Research Articles

Model based security verification of protocol implementation

Finite transition models such as Automata, Labeled Transition System, have been widely used to model and analyze the complex system and protocol implementations. Those methods model the systems with states and transitions, and present them with a reachable graph. Properties of the systems such as conformance, robustness, and interoperability, can be verified through the test cases, which are generated from those reachable graphs. But these methods are still hard to adopt the requirements of security protocols, because first of all, in the classic definition of transition model, the non-negligible security properties (such as nonce, encryption etc.) cannot be described and analyzed. In addition, security protocols usually need to concern the malicious actions from the probable intruders, which is also an obstacle to classical transition based modeling. In this article, we firstly extend the standard Input Output Labeled Transition System (IOLTS) model to a secure and glued IOLTS (SG IOLTS) model, which can include security properties and their associated security functions. Then we propose a general finite intruder model, which makes the final reachable graph of the whole system contains the malicious actions from intruders. A corresponding algorithm for automatic test generation is also given and an example of verifying Needham-Schroeder-Lowe (NSL) protocol is proposed in the end.

Chronic psychosocial stress impairs early LTP but not late LTP in the dentate gyrus of at-risk rat model of Alzheimer׳s disease

The CA1 and dentate gyrus regions of the hippocampus are physically and functionally closely related but they react differently to insults. This study examined the effect of chronic psychosocial stress on the dentate gyrus of an at-risk (preclinical) rat model of Alzheimer׳s disease (subAβ rats). Chronic psychosocial stress was produced using a rat intruder model. The at-risk rat model of Alzheimer׳s disease was created by osmotic pump infusion of sub-pathological dose of Aβ (160pmol Aβ1–42/day i.c.v) for 14 days. Electrophysiological methods were used to evoke and record early and late phase LTP in the dentate gyrus of anesthetized rats, and immunoblotting was used to measure levels of memory-related signaling molecules in the same region. Electrophysiological and molecular tests in the dentate gyrus showed that subAβ rats or stressed rats were not different from control rats. However, when the subAβ rats were chronically stressed, the combined treatments severely suppressed early phase LTP without affecting the late phase LTP of dentate gyrus. Additionally, in the chronically stressed subAβ rats the expected elevation of levels of phosphorylated CaMKII did not materialize after expression of early phase LTP suggesting impaired phosphorylation, which may explain the severely blocked early phase LTP.

Chronic Stress Decreases Basal Levels of Memory-Related Signaling Molecules in Area CA1 of At-Risk (Subclinical) Model of Alzheimer's Disease.

An important factor that may affect the severity and time of onset of Alzheimer's disease (AD) is chronic stress. Epidemiological studies report that chronically stressed individuals are at an increased risk for developing AD. The purpose of this study was to reveal whether chronic psychosocial stress could hasten the appearance of AD symptoms including changes in basal levels of cognition-related signaling molecules in subjects who are at risk for the disease. We investigated the effect of chronic psychosocial stress on basal levels of memory-related signaling molecules in area CA1 of subclinical rat model of AD. The subclinical symptomless rat model of AD was induced by osmotic pump continuous intracerebroventricular (ICV) infusion of 160 pmol/day Aβ1-42 for 14 days. Rats were chronically stressed using the psychosocial stress intruder model. Western blot analysis of basal protein levels of important signaling molecules in hippocampal area CA1 showed no significant difference between the subclinical AD rat model and control rat. Following six weeks of psychosocial stress, molecular analysis showed that subclinical animals subjected to stress have significantly reduced basal levels of p-CaMKII and decreased p-CaMKII/t-CaMKII ratio as well as decreased basal levels of p-CREB, total CREB, and BDNF. The present results suggest that these changes in basal levels of signaling molecules may be responsible for impaired learning, memory, and LTP in this rat model, which support the proposition that chronic stress may accelerate the emergence of AD in susceptible individuals.

Analysis of two authorization protocols using Colored Petri Nets

To prevent unauthorized access to protected trusted platform module (TPM) objects, authorization protocols, such as the object-specific authorization protocol (OSAP), have been introduced by the trusted computing group (TCG). By using OSAP, processes trying to gain access to the protected TPM objects need to prove their knowledge of relevant authorization data before access to the objects can be granted. Chen and Ryan's 2009 analysis has demonstrated OSAP's authentication vulnerability in sessions with shared authorization data. They also proposed the Session Key Authorization Protocol (SKAP) with fewer stages as an alternative to OSAP. Chen and Ryan's analysis of SKAP using ProVerif proves the authentication property. The purpose of this paper was to examine the usefulness of Colored Petri Nets (CPN) and CPN Tools for security analysis. Using OSAP and SKAP as case studies, we construct intruder and authentication property models in CPN. CPN Tools is used to verify the authentication property using a Dolev---Yao-based model. Verification of the authentication property in both models using the state space tool produces results consistent with those of Chen and Ryan.

Novel mechanistic insights into treadmill exercise based rescue of social defeat-induced anxiety-like behavior and memory impairment in rats

Social defeat (SD) induced stress causes physiological and behavioral deficits in rodents, including depression and anxiety-like behaviors, as well as memory impairment. Anxiolytic and mood elevating effects of physical exercise are also known. However, rescue effect of physical exercise in social defeat-induced anxiety, depression or memory impairment has not been addressed. The role of epigenetic mechanisms that potentially contribute to these rescue or protective effects is also not known. The present study investigated the effect of moderate treadmill exercise on anxiety-like behavior and memory function in rats subjected to SD using a modified version of the resident–intruder model for social stress (defeat). Changes in histone acetylation and histone-modifying enzymes were examined in hippocampus, amygdala and frontal cortex which are considered critical for anxiety, depression and cognition. Sprague Dawley rats were randomly assigned in four groups; control, exercised, social defeat, social defeat and exercise. At the end of the SD or control exposure lasting 30min daily for 7days, one group of SD rats was subjected to treadmill exercise for 2weeks, whereas the other SD group was handled without exercise. Anxiety-like behavior tests and radial arm water maze test suggested that moderate treadmill exercise rescued social defeat induced anxiety-like behavior and memory impairment. Moreover, exercise normalized SD-induced increase in oxidative stress, most likely by adjusting antioxidant response. Our data suggests involvement of epigenetic mechanisms including histone acetylation of H3 and modulation of methyl-CpG-binding in the hippocampus that might contribute to the rescue effects of exercise in SD-induced behavioral deficits in rats.

Extending TLS with Mutual Attestation for Platform Integrity Assurance

Normally, secure communication between client-server applications is established using secure channel technologies such as Transport Layer Security (TLS). TLS is cryptographic protocol which ensures secure transmission of data and authenticity of communication at each endpoint platform. However, the protocol does not provide any trustworthiness assurance of the involved endpoint. This paper incorporates remote attestation in the TLS key exchange protocol to solve this issue.The proposed embedded attestation extension in TLS protocol will provide assurance of sender's platforms integrity to receiver, and vice versa.The CA responsibility in TLS is replaced using own Trusted Certificate Authority (TCA) in our protocol. The credibility of the proposed protocol is studied to secure against replay attack and collusion attack. The proof is performed using AVISPA with High Level Protocol Specification (HLPSL) through Dolev-Yao intruder model implementation of the proposed protocol.

Surveillance using non‐stealthy sensors: A new intruder model

ABSTRACTWe study the problem of intruder tracking with non‐stealthy sensors, i.e., sensors whose ON/OFF state can be detected by an intruder, sometimes in advance. The sensor field is assumed to be operating with a sleep schedule to conserve energy. Both motion sensors and presence sensors are considered. We provide a rigorous basis for the study of this scenario by defining a new intruder model, the Ideal Intruder, that knows the entire sleep schedule of all the sensors in the field. More realistic intruders that have spatially and temporally limited knowledge of the sensor states are also defined. We study the well‐known Random Independent Sleep (RIS) scheduling scheme with a single parameter p, giving mathematical bounds for the ideal intruder's crossing time in the motion sensor case and showing that the crossing probability in the presence sensor case undergoes a sharp transition as p increases. Further, we show that non‐ideal intruders perform almost as well as the ideal intruder against RIS. Motivated by this finding and by the comparison between Barrier Coverage and RIS, we define a new sleep scheduling scheme, Spotlight, that is more robust to faults than Barrier Coverage and more effective than RIS. But more than that, Spotlight is shown to be specifically suited to the non‐stealthy case because a non‐ideal intruder, that is, one with limited information performs significantly worse against it than the ideal intruder. Spotlight, therefore, apart from being a novel and interesting sleep scheduling scheme in its own right, also illustrates the power of the analytical framework we introduce in this paper. Copyright © 2013 John Wiley & Sons, Ltd.

Role of α7- and α4β2-nAChRs in the neuroprotective effect of nicotine in stress-induced impairment of hippocampus-dependent memory

We have previously shown that nicotine prevents stress-induced memory impairment. In this study, we have investigated the role of α7- and α4β2-nicotinic acetylcholine receptors (nAChRs) in the protective effect of nicotine during chronic stress conditions. Chronic psychosocial stress was induced using a form of rat intruder model. During stress, specific antagonist for either α7-nAChRs [methyllycaconitine (MLA)] or α4β2-nAChRs [dihydro-β-erythroidine (DHβE)] was infused into the hippocampus using a 4-wk osmotic pump at a rate of 82μg/side.d and 41μg/side.d, respectively. Three weeks after the start of infusion, all rats were subjected to a series of cognitive tests in the radial arm water maze (RAWM) for six consecutive days or until the animal reached days to criterion (DTC) in the fourth acquisition trial and in all memory tests. DTC is defined as the number of days the animal takes to make no more than one error in three consecutive days. In the short-term memory test, MLA-infused stressed/nicotine-treated rats made similar errors to those of stress and significantly more errors compared to those of stress/nicotine, nicotine or control groups. This finding was supported by the DTC values for the short memory tests. Thus, MLA treatment blocked the neuroprotective effect of nicotine during chronic stress. In contrast, DHβE infusion did not affect the RAWM performance of stress/nicotine animals. These results strongly suggest the involvement of α7-nAChRs, but not α4β2-nAChRs, in the neuroprotective effect of chronic nicotine treatment during chronic stress conditions.

Enkephalin and dynorphin mRNA expression are associated with resilience or vulnerability to chronic social defeat stress

There are important and enduring differences between individuals in the magnitude of all aspects of the stress response. Among the neuropeptide systems, the endogenous opioids enkephalin (ENK) and dynorphin (DYN), are very interesting candidates to participate in the naturally occurring variations in coping styles and to determine the individual capacity for adaptation during chronic stress exposure. Under chronic social stress exposure, we hypothesize that changes in the ENKergic vs DYNergic neuronal systems within specific nuclei of the basal forebrain contribute to naturally occurring variations in coping styles and will determine individual capacities for stress adaptation. Sprague–Dawley rats were exposed to a resident–intruder model of defeat for 7days. The average latency to be defeated over seven consecutive days was calculated for each intruder rat. Based on this distribution, we chose an average defeat latency of 350s as a cutoff criterion to define resilient and vulnerable rats. A subpopulation assumed a subordinate posture in a relatively short latency (<350s, SL) and the other subpopulation resisted defeat resulting in longer latencies (>350s, LL) to assume this posture and were identified as being vulnerable and resilient respectively. Rats were euthanized 24h after the last stress session. ENK mRNA expression was lower in the basolateral nucleus of the amygdala in vulnerable compared to control and resilient individuals. In contrast, there was no difference between resilient and control individuals. DYN mRNA is increased only within the dorsal and medial shell of the NAc of vulnerable rats compared to control individuals. There was no difference between resilient and control individuals. DYN mRNA is increased in resilient individuals in the central area of the striatum, caudal part, compared to control individuals. DYN is also increased in medial area of the striatum, caudal part in resilient and vulnerable compared to control individuals. These results have broad implications for understanding the functional roles of opioid neurotransmission following repeated social stress and suggest that ENK could facilitate the adaptation of behavioral responses by opposition to the DYN neurotransmission that appears to promote maladaptive behavioral response to chronic social stress.

Manganese-enhanced magnetic resonance imaging (MEMRI) reveals brain circuitry involved in responding to an acute novel stress in rats with a history of repeated social stress

Responses to acute stressors are determined in part by stress history. For example, a history of chronic stress results in facilitated responses to a novel stressor and this facilitation is considered to be adaptive. We previously demonstrated that repeated exposure of rats to the resident–intruder model of social stress results in the emergence of two subpopulations that are characterized by different coping responses to stress. The submissive subpopulation failed to show facilitation to a novel stressor and developed a passive strategy in the Porsolt forced swim test. Because a passive stress coping response has been implicated in the propensity to develop certain psychiatric disorders, understanding the unique circuitry engaged by exposure to a novel stressor in these subpopulations would advance our understanding of the etiology of stress-related pathology. An ex vivo functional imaging technique, manganese-enhanced magnetic resonance imaging (MEMRI), was used to identify and distinguish brain regions that are differentially activated by an acute swim stress (15min) in rats with a history of social stress compared to controls. Specifically, Mn2+ was administered intracerebroventricularly prior to swim stress and brains were later imaged ex vivo to reveal activated structures. When compared to controls, all rats with a history of social stress showed greater activation in specific striatal, hippocampal, hypothalamic, and midbrain regions. The submissive subpopulation of rats was further distinguished by significantly greater activation in amygdala, bed nucleus of the stria terminalis, and septum, suggesting that these regions may form a circuit mediating responses to novel stress in individuals that adopt passive coping strategies. The finding that different circuits are engaged by a novel stressor in the two subpopulations of rats exposed to social stress implicates a role for these circuits in determining individual strategies for responding to stressors. Finally, these data underscore the utility of ex vivo MEMRI to identify and distinguish circuits engaged in behavioral responses.

Chronic Caffeine Treatment Prevents Stress-Induced LTP Impairment: the Critical Role of Phosphorylated CaMKII and BDNF

Caffeine has been reported to enhance cognition in animal and humans. Additionally, caffeine alleviates cognitive impairment associated with a number of disorders including Alzheimer's disease. The lipophilic nature of caffeine allows for rapid absorption into the bloodstream where it freely crosses the blood-brain barrier. Caffeine promotes dendritic spine growth in cultured hippocampal neurons, which suggests a neuroprotective effect. We examined the effect of chronic caffeine treatment on stress-induced suppression of long-term potentiation (LTP) and impairment of molecules of its signaling cascade. Rats were subjected to daily stress using the psychosocial stress paradigm (intruder model), in vivo recordings from area CA1 of the hippocampus of adult rat, and immunoblot analysis of essential signaling molecules. Caffeine prevented stress-induced LTP impairment. Western blot analysis showed reduction of the basal levels of the phosphorylated calcium calmodulin kinase II (P-CAMKII), total CaMKII, and brain-derived neurotrophic factor (BDNF) in area CA1 of stressed rats. These reductions were prevented by chronic caffeine treatment (0.33mg/L in drinking water). In addition, caffeine prevented the upregulation of calcineurin levels in stressed rats. High-frequency stimulation (HFS) normally increased P-CaMKII, total CaMKII, and calcineurin levels in control as well as in caffeine-treated stressed rats. However, in stressed rats, the same HFS induced increases in the levels of total CaMKII and calcineurin, but not those of P-CaMKII. The levels of signaling molecules may not reflect activities of these molecules. It appears that the neuroprotective effect of caffeine involves preservation of the levels of essential kinases and phosphatases in stressed rats. This may include preservation of basal levels of BDNF by chronic caffeine treatment in stressed animals. These findings highlight the critical role of P-CaMKII and BDNF in caffeine-induced prevention of stress-induced LTP impairment.

Timed protocol insecurity problem is NP-complete

In this paper we study the protocol insecurity problem for time-dependent security protocols under the finite number of sessions’ assumption, extending to the timed case, previous results obtained for the same problem in the untimed case. In particular, we propose a timed specification language, which allows to model temporal features typically involved in the implementation of security protocols. We introduce a stronger version of the Dolev–Yao intruder, by allowing it to generate new timestamps which can affect the execution of a protocol sensitive to their temporal validity. We prove that this temporal extension together with the increased power of the intruder model do not affect the complexity of the protocol insecurity problem, which remains NP-complete as in the untimed case.

Chronic psychosocial stress enhances long‐term depression in a subthreshold amyloid‐beta rat model of Alzheimer’s disease

In addition to genetic aspects, environmental factors such as stress may also play a critical role in the etiology of the late onset, sporadic Alzheimer's disease (AD). The present study examined the effect of chronic psychosocial stress in a sub-threshold Aβ (subAβ) rat model of AD on long-term depression by two techniques: electrophysiological recordings of synaptic plasticity in anesthetized rats, and immunoblot analysis of memory- and AD-related signaling molecules. Chronic psychosocial stress was induced using a rat intruder model. The subAβ rat model of AD, which was intended to represent outwardly normal individuals with a pre-disposition to AD, was induced by continuous infusion of 160 pmol/day Aβ₁₋₄₂ via a 14-day i.c.v. osmotic pump. Results from electrophysiological recordings showed that long-term depression evoked in stress/subAβ animals was significantly enhanced compared with that in animals exposed to stress or subAβ infusion alone. Molecular analysis of various signaling molecules 1 h after induction of long-term depression revealed an increase in the levels of calcineurin and phosphorylated CaMKII in groups exposed to stress compared with other groups. The levels of the brain-derived neurotrophic factor (BDNF) were significantly decreased in stress/subAβ animals but not in stress or subAβ animals. In addition, the levels of beta-site amyloid precursor protein cleaving enzyme were markedly increased in stress/subAβ. These findings suggest that chronic stress may accelerate the impairment of synaptic plasticity and consequently cognition in individuals 'at-risk' for AD.

Chronic psychosocial stress accelerates impairment of long‐term memory and late‐phase long‐term potentiation in an at‐risk model of Alzheimer's disease

Although it is generally agreed that Aβ contributes to the pathogenesis of AD, its precise role in AD and the reason for the varying intensity and time of onset of the disease have not been elucidated. In addition to genetic factors, environmental issues such as stress may also play a critical role in the etiology of AD. This study examined the effect of chronic psychosocial stress in an at-risk (treatment with a subpathogenic dose of Aβ; "subAβ") rat model of AD on long-term memory by three techniques: memory tests in the radial arm water maze, electrophysiological recordings of synaptic plasticity in anesthetized rats, and immunoblot analysis of learning- and long-term memory-related signaling molecules. Chronic psychosocial stress was induced using a rat intruder model. The subAβ rat model of AD was induced by continuous infusion of 160 pmol/day Aβ(1-42) via a 14-day i.c.v. osmotic pump. All tests showed that subAβ rats were not different from control rats. Result from behavioral tests and electrophysiological recordings showed that infusion of subAβ in chronically stressed rats (stress/subAβ group) caused significant impairment of cognitive functions and late-phase long-term potentiation (L-LTP). Molecular analysis of various signaling molecules after expression of L-LTP, revealed an increase in the levels of p-CREB in control, stress, and subAβ rats, but not in the stress/subAβ rats. These findings suggest that the chronic stress-induced molecular alteration may accelerate the impairment of cognition and synaptic plasticity in individuals "at-risk" for AD.

Synthesis of attack actions using model checking for the verification of security protocols

AbstractModel checking cryptographic protocols have evolved to a valuable method for discovering counterintuitive security flaws, which makes it possible for a hostile agent to subvert the goals of the protocol. Published works and existing security analysis tools are usually based on general intruder models that embody at least some aspects of the seminal work of Dolev–Yao, in an attempt to detect failures of secrecy. In this work, we propose an alternative intruder model, which is based on a thorough analysis of how potential attacks might proceed. We introduce an intruder model that provides an open‐ended base for the integration of multiple basic attack tactics. Those attack tactics have the possibility to be combined, in a way to compose complex attack actions that require a number of procedural steps from the intruder's side, such as a Denial of Service attack. In our model checking approach, protocol correctness is checked by appropriate user‐supplied assertions or reachability of invalid end states. The analyst can express security properties of specific attack actions that are not restricted to safety violations captured by a generic model checker. The described intruder model methodology was implemented within the SPIN model checker for verifying two security protocols, Micromint and PayWord. Copyright © 2009 John Wiley &amp; Sons, Ltd.

Aircraft Collision Avoidance Using Monte Carlo Real-Time Belief Space Search

The aircraft collision avoidance problem can be formulated using a decision-theoretic planning framework where the optimal behavior requires balancing the competing objectives of avoiding collision and adhering to a flight plan. Due to noise in the sensor measurements and the stochasticity of intruder state trajectories, a natural representation of the problem is as a partially-observable Markov decision process (POMDP), where the underlying state of the system is Markovian and the observations depend probabilistically on the state. Many algorithms for finding approximate solutions to POMDPs exist in the literature, but they typically require discretization of the state and observation spaces. This paper investigates the introduction of a sample-based representation of state uncertainty to an existing algorithm called Real-Time Belief Space Search (RTBSS), which leverages branch-and-bound pruning to make searching the belief space for the optimal action more efficient. The resulting algorithm, called Monte Carlo Real-Time Belief Space Search (MC-RTBSS), is demonstrated on encounter scenarios in simulation using a beacon-based surveillance system and a probabilistic intruder model derived from recorded radar data.

Channel abstractions for network security

Process algebraic techniques for distributed systems are increasingly being targeted at identifying abstractions that are adequate for both high-level programming and specification and security analysis and verification. Drawing on our earlier work in Bugliesi and Focardi, (2008), we investigate the expressive power of a core set of security and network abstractions that provide high-level primitives for specifying the honest principals in a network, while at the same time enabling an analysis of the network-level adversarial attacks that may be mounted by an intruder.We analyse various bisimulation equivalences for security that arise from endowing the intruder with: (i)different adversarial capabilities; and(ii)increasingly powerful control over the interaction among the distributed principals of a network. By comparing the relative strength of the bisimulation equivalences, we obtain a direct measure of the intruder's discriminating power, and hence of the expressiveness of the corresponding intruder model.

Chronic psychosocial stress triggers cognitive impairment in a novel at-risk model of Alzheimer's disease

Although it is generally accepted that Aβ contributes to the pathogenesis of Alzheimer's disease (AD), other factors that impact the severity and time of onset of the disease are not well known. Aside from genetic factors, environmental factors such as stress may also play a critical role in the manifestation of AD. The present study examined the effect of chronic psychosocial stress in an at-risk, subthreshold Aβ (subAβ) rat model of AD by three approaches: learning and memory tests in the radial arm water maze, electrophysiological recordings of long-term potentiation (LTP) in anesthetized rats, and immunoblot analysis of learning- and memory-related signaling molecules. Chronic psychosocial stress was induced using a rat intruder model. The subAβ rat model of AD was induced by continuous i.c.v. infusion of 160 pmol/day Aβ 1-42 via a 14-day osmotic pump. Behavioral tests and electrophysiological recordings showed that subAβ rats were not significantly different from control rats. However, chronically stressed subAβ rats showed more significant impairment of cognitive functions and early-phase LTP (E-LTP) than that caused by stress alone. Molecular analysis of essential signaling molecules after induction of E-LTP revealed an increase in the levels of p-CaMKII in control as well as subAβ infused rats, but not in stressed or stressed at-risk rats. In addition, compared to unstimulated control, the levels of both total CaMKII and calcineurin were increased in all stimulated animals groups after HFS. These findings suggest that the stress-induced alterations may accelerate the impairment of cognition and synaptic plasticity in individuals “at-risk” for AD.

Chronic Stress Accelerates and Intensifies Aß-induced Alzheimer’s-disease-like Pathogenesis in Rat Models

Apart from genetic factors, environmental factors such as stress may also play a critical role in the manifestation of Alzheimer’s disease (AD). We studied the impact of chronic psychosocial stress in two amyloid-beta (Aβ) rat models of AD by three approaches: learning and memory tests in the radial arm water maze, electrophysiological recordings of long-term potentiation (LTP) in anesthetized rats, and immunoblot analysis of synaptic plasticity- and cognition-related signaling molecules. The first Aβ rat model, representing established AD, was induced by continuous intracerebroventricular (ICV) infusion of a pathogenic dose of Aβ peptides via a 14-day osmotic pump. In this AD model, chronic stress intensified cognitive deficits, produced more depression of LTP, and accentuated the reduction of signaling molecule levels compared with the established model alone. The second model represents subjects that are clinically normal but are at risk for AD, and was induced by ICV infusion of a sub-threshold (sub-Aβ) dose of Aβ peptides. Chronic psychosocial stress was induced using a rat intruder model. Various tests showed that sub-Aβ rats were not significantly different from control rats. However, chronically stressed sub-Aβ rats showed more significant impairment of cognitive functions and early-phase LTP than that caused by stress alone. Molecular analysis revealed marked disturbances in the levels of essential signaling molecules in the stressed AD at-risk rats. These findings suggest that chronic stress may profoundly accelerate and intensify the impairment of cognition and synaptic plasticity in individuals at risk for AD and those with established AD, respectively. Possible mechanisms for the effect of chronic stress are discussed.

An intruder model with message inspection for model checking security protocols

Model checking security protocols is based on an intruder model that represents the eavesdropping or interception of the exchanged messages, while at the same time performs attack actions against the ongoing protocol session(s). Any attempt to enumerate all messages that can be deduced by the intruder and the possible actions in all protocol steps results in an enormous branching of the model's state-space. In current work, we introduce a new intruder model that can be exploited for state-space reduction, optionally in combination with known techniques, such as partial order and symmetry reduction. The proposed intruder modeling approach called Message Inspection (MI) is based on enhancing the intruder's knowledge with metadata for the exchanged messages. In a preliminary simulation run, the intruder tags the analyzed messages with protocol-specific values for a set of predefined parameters. This metadata is used to identify possible attack actions, for which it is a priori known that they cannot cause a security violation. The MI algorithm selects attack actions that can be discarded, from an open-ended base of primitive attack actions. Thus, model checking focuses only on attack actions that may disclose a security violation. The most interesting consequence is a non-negligible state-space pruning, but at the same time our approach also allows customizing the behavior of the intruder model, in order e.g. to make it appropriate for model checking problems that involve liveness. We provide experimental results obtained with the SPIN model checker, for the Needham–Schroeder security protocol.