Who Can Find My Devices? Security and Privacy of Apple's Crowd-Sourced Bluetooth Location Tracking System

Overnight, Apple has turned its hundreds-of-million-device ecosystem into the world's largest crowd-sourced location tracking network called offline finding (OF). OF leverages online finder devices to detect the presence of missing offline devices using Bluetooth and report an approximate location back to the owner via the Internet. While OF is not the first system of its kind, it is the first to commit to strong privacy goals. In particular, OF aims to ensure finder anonymity, untrackability of owner devices, and confidentiality of location reports. This paper presents the first comprehensive security and privacy analysis of OF. To this end, we recover the specifications of the closed-source OF protocols by means of reverse engineering. We experimentally show that unauthorized access to the location reports allows for accurate device tracking and retrieving a user's top locations with an error in the order of 10 meters in urban areas. While we find that OF's design achieves its privacy goals, we discover two distinct design and implementation flaws that can lead to a location correlation attack and unauthorized access to the location history of the past seven days, which could deanonymize users. Apple has partially addressed the issues following our responsible disclosure. Finally, we make our research artifacts publicly available.Comment: Accepted at Privacy Enhancing Technologies Symposium (PETS) 202

Who Can Find My Devices? Security and Privacy of Apple’s Crowd-Sourced Bluetooth Location Tracking System

Overnight, Apple has turned its hundreds-of-million-device ecosystem into the world’s largest crowd-sourced location tracking network called o~ine finding (OF). OF leverages online finder devices to detect the presence of missing o~ine devices using Bluetooth and report an approximate location back to the owner via the Internet. While OF is not the first system of its kind, it is the first to commit to strong privacy goals. In particular, OF aims to ensure finder anonymity, prevent tracking of owner devices, and confidentiality of location reports. This paper presents the first comprehensive security and privacy analysis of OF. To this end, we recover the specifications of the closed-source OF protocols by means of reverse engineering. We experimentally show that unauthorized access to the location reports allows for accurate device tracking and retrieving a user’s top locations with an error in the order of 10 meters in urban areas. While we find that OF’s design achieves its privacy goals, we discover two distinct design and implementation flaws that can lead to a location correlation attack and unauthorized access to the location history of the past seven days, which could deanonymize users. Apple has partially addressed the issues following our responsible disclosure. Finally, we make our research artifacts publicly available

SUCLG2 identified as both a determinator of CSF Aβ1-42 levels and an attenuator of cognitive decline in Alzheimer's disease

Cerebrospinal fluid amyloid-beta 1-42 (Aβ1-42) and phosphorylated Tau at position 181 (pTau181) are biomarkers of Alzheimer's disease (AD). We performed an analysis and meta-analysis of genome-wide association study data on Aβ1-42 and pTau181 in AD dementia patients followed by independent replication. An association was found between Aβ1-42 level and a single-nucleotide polymorphism in SUCLG2 (rs62256378) (P = 2.5×10−12). An interaction between APOE genotype and rs62256378 was detected (P = 9.5 × 10−5), with the strongest effect being observed in APOE-ε4 noncarriers. Clinically, rs62256378 was associated with rate of cognitive decline in AD dementia patients (P = 3.1 × 10−3). Functional microglia experiments showed that SUCLG2 was involved in clearance of Aβ1-4

Convergent genetic and expression data implicate immunity in Alzheimer's disease

Background Late–onset Alzheimer's disease (AD) is heritable with 20 genes showing genome wide association in the International Genomics of Alzheimer's Project (IGAP). To identify the biology underlying the disease we extended these genetic data in a pathway analysis. Methods The ALIGATOR and GSEA algorithms were used in the IGAP data to identify associated functional pathways and correlated gene expression networks in human brain. Results ALIGATOR identified an excess of curated biological pathways showing enrichment of association. Enriched areas of biology included the immune response (p = 3.27×10-12 after multiple testing correction for pathways), regulation of endocytosis (p = 1.31×10-11), cholesterol transport (p = 2.96 × 10-9) and proteasome-ubiquitin activity (p = 1.34×10-6). Correlated gene expression analysis identified four significant network modules, all related to the immune response (corrected p 0.002 – 0.05). Conclusions The immune response, regulation of endocytosis, cholesterol transport and protein ubiquitination represent prime targets for AD therapeutics

Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson’s disease (PD) and Alzheimer’s disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues

Zeitenwende für Europas Sicherheitsordnung: Entwicklungsoptionen in drei Skizzen

Der von Russland im Februar begonnene Angriffskrieg auf die Ukraine hat die bisherige europäische Sicherheitsordnung zerstört. Bereits jetzt muss die von der Bundesregierung proklamierte Zeitenwende in der deutschen Außen- und Sicherheitspolitik eine neue Ordnung ins Auge fassen und gestalten, um erfolgreich zu sein. Schlüsselfaktoren sind die Einigkeit Europas in strategischen Politikfeldern sowie Russlands Positionierung gegenüber dem Rest Europas. Die drei Zukunftsoptionen - Konfrontation, Koexistenz oder Kooperation - identifizieren die Grundlagen für ein starkes Europa

Effect of Minocycline on Depressive Symptoms in Patients With Treatment-Resistant Depression

IMPORTANCE Insufficient treatment response and resulting chronicity constitute a major problem in depressive disorders. Remission rates range as low as 15% to 40% and treatment-resistant depression (TRD) is associated with low-grade inflammation, suggesting anti-inflammatory interventions as a rational treatment strategy. Minocycline, which inhibits microglial activation, represents a promising repurposing candidate in the treatment of TRD. OBJECTIVE To determine whether 6 weeks of minocycline as add-on to antidepressant treatment as usual can significantly reduce depressive symptoms in patients with TRD. DESIGN, SETTING, AND PARTICIPANTS The study was conducted in Germany and designed as a multicenter double-blind randomized clinical trial (RCT) of 200 mg/d minocycline treatment over a course of 6 weeks with a 6-month follow-up. Participants were recruited from January 2016 to August 2020 at 9 university hospitals that served as study sites. Key inclusion criteria were a diagnosis of major depressive disorder (according to Diagnostic and Statistical Manual of Mental Disorders [Fifth Edition] criteria), severity of depressive symptoms on the Hamilton Depression Rating Scale (HAMD-17) greater than or equal to 16 points, aged 18 to 75 years, body mass index 18 to 40, Clinical Global Impression Scale (CGI-S) greater than or equal to 4, failure to adequately respond to an initial antidepressant standard medication as per Massachusetts General Hospital Antidepressant Treatment History Questionnaire, and stable medication for at least 2 weeks. A total of 258 patients were screened, of whom 173 were randomized and 168 were included into the intention-to-treat population. Statistical analysis was performed from April to November 2020. INTERVENTIONS Participants were randomized (1:1) to receive adjunct minocycline (200 mg/d) or placebo for 6 weeks. MAIN OUTCOMES AND MEASURES Primary outcome measure was the change in Montgomery-Asberg Depression Rating Scale (MADRS) score from baseline to week 6 analyzed by intention-to-treat mixed model repeated measures. Secondary outcome measures were response, remission, and various other clinical rating scales. RESULTS Of 173 eligible and randomized participants (84 randomized to minocycline and 89 randomized to placebo), 168 formed the intention-to-treat sample (79 [47.0%] were women, 89 [53.0%] were men, 159 [94.6%] were White, 9 [6.4%] were of other race and ethnicity, including Asian and unknown ethnicity), with 81 in the minocycline group and 87 in the placebo group. The mean (SD) age was 46.1 (13.1) years, and the mean (SD) MADRS score at baseline was 26.5 (5.0). There was no difference in rates of completion between the minocycline (83.3% [70 of 81]) and the placebo group (83.1% [74 of 87]). Minocycline treatment did not alter the course of depression severity compared with placebo as assessed by a decrease in MADRS scores over 6 weeks of treatment (1.46 [-1.04 to 3.96], P = .25). Minocycline treatment also exhibited no statistically significant effect on secondary outcomes. CONCLUSIONS AND RELEVANCE In this large randomized clinical trial with minocycline at a dose of 200 mg/d added to antidepressant treatment as usual for 6 weeks, minocycline was well tolerated but not superior to placebo in reducing depressive symptoms in patients with TRD. The results of this RCT emphasize the unmet need for therapeutic approaches and predictive biomarkers in TRD