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Parkinson’s disease (PD) is the fastest-growing neurological disease in the world. A key challenge in PD is tracking
disease severity, progression, and medication response. Existing methods are semisubjective and require visiting
the clinic. In this work, we demonstrate an effective approach for assessing PD severity, progression, and medication
response at home, in an objective manner. We used a radio device located in the background of the home. The
device detected and analyzed the radio waves that bounce off people’s bodies and inferred their movements and gait
speed. We continuously monitored 50 participants, with and without PD, in their homes for up to 1 year. We collected
over 200,000 gait speed measurements. Cross-sectional analysis of the data shows that at-home gait speed strongly
correlates with gold-standard PD assessments, as evaluated by the Movement Disorder Society-Sponsored Revision
Liu et al., Sci. Transl. Med. 14, eadc9669 (2022) 21 September 2022 1 of 13
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A B C
Our sensor
Our sensor
Disease progression
Fig. 1. System overview. (A) Our sensor operates like a low-power radar. It transmits wireless signals that are only 1/1000 the power of a home Wi-Fi router, and passively
and continuously collects signals reflected from nearby people. (B) The collected radio signals are analyzed to extract participants’ movement trajectories and gait speeds.
(C) Using the large amount of trajectory and gait data collected across time, we evaluate PD disease severity, disease progression, and patients’ response to medications.
Table 1. Demographical and clinical characteristics. Unless otherwise specified, values are at baseline.
PD group (n = 34) Control group (n = 16)
age-matched control subjects) continuously in their homes. The with their lives. Our results also motivate the use of in-home
first study enrolled 20 participants, who were monitored for 2 months. radio-based gait monitoring to study other diseases associated with
The remaining participants (60%) are enrolled in an ongoing 2-year gait and motor dysfunction, such as Huntington’s disease (13, 14)
observational study. The evaluation demonstrated that unscripted and multiple sclerosis (15).
gait measurements collected using our radio device provide a valid marker
of PD severity, progression, and medication response.
Now, most of drug clinical trials and medical care are limited to RESULTS
subjective episodic PD measurements, typically conducted in a clinic. Participant characteristics
In contrast, the approach described here demonstrates the feasibility We enrolled 50 individuals, including 34 with PD [age 69.4 (7.6)
of assessing individual patients in their natural living environments to years, 26% women] and 16 without PD [age 66.4 (13.0) years, 50%
obtain objective, detailed, and clinically meaningful measurements of women]. Among them, 40% were observed for 8 weeks, whereas
their disease. Furthermore, these measurements can be collected in a the rest were enrolled in an ongoing longitudinal study and were
passive manner without asking patients to wear sensors or interfering monitored for up to 1 year. Table 1 summarizes the demographics
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A B
1.00 1.0
0.98
0.9
0.7
Test-retest reliability
0.90
0.6
0.5
1 2 3 4 5 6 7 8 9 10 11 12 13 14
0.85
Size of intervals (days)
1.1
0.80 1.0
0.75
95% CI 0.8
0.7
0.70
0 2 4 6 8 10 12 14 0.6
1 2 3 4 5 6 7 8 9 10 11 12 13 14
Size of intervals (days) Size of intervals (days)
and clinical characteristics of the participants, and fig. S1 provides In-home gait speed as a marker of PD severity
more details about their MDS-UPDRS and ON-OFF behavior. In Several prior studies have shown that gait speed is associated with
total, we collected over 200,000 gait speed measurements. The mean important medical outcomes, such as health status, cognitive func-
(SD) baseline in-home gait speed among those with PD was 0.70 tion, dementia, and mortality (17–20). In this study, we investigated
(0.085) m/s, and that among those without PD was 0.91 (0.075) m/s. whether gait speed measured passively at home provides a clinically
Thus, individuals with PD had about 23% lower in-home gait speed meaningful assessment of PD severity. To do so, we compared in-
than the control cohort (t = −8.10, P < 0.001). home gait speed against common measures of PD severity such as
the MDS-UPDRS part III subscore and total score. Since the MDS-
Reliability of in-home gait speed measurements UPDRS is assessed during ON time, we use the 75th percentile gait
Any measurement incurs some variability that is independent from speed for this correlation to bias the gait speed toward the ON state.
the disease and is due to noise in the measuring device or measure- The results in Fig. 3 (A and B) show that among PD and control
ment condition. For example, the person may walk slower than usual participants, in-home gait speed is strongly correlated with both the
if they are talking on the phone or may walk faster if they are trying MDS-UPDRS total score (n = 50, r = −0.83, P < 0.001) and the part
to reach a ringing alarm. Further, the radio device may introduce III subscore (n = 50, r = −0.86, P < 0.001). Further, a subanalysis
some noise. Thus, it is important to average or aggregate individual focused on the axial symptoms as measured by the sum of items 1
gait measurements to obtain a consistent measurement that reflects and 9 to 13 in the MDS-UPDRS part III reveals that they, too, are
the health status of the individual. To estimate the proper aggrega- strongly correlated with in-home gait speed (n = 50, r = −0.83, P < 0.001).
tion window, we computed the test-retest reliability (16). The re- We also used a covariate-adjusted linear model to validate that the
sults reported in Fig. 2A show that the test-retest reliability of gait correlation between in-home gait speed and the MDS-UPDRS,
speed increases with longer averaging windows, and both the aver- both total and part III, is not affected by confounding factors such as
age and confidence interval (CI) cross the 95% threshold (n = 50) age, gender, or comorbidities (table S1). Given that MDS-UPDRS
for a window size of only 14 days [intraclass correlation coefficient is the key metric for evaluating disease severity in PD clinical trials,
(ICC), 0.98; 95% CI, 0.97 to 0.99]. We also considered an alternative this result demonstrates that in-home passive gait speed measure-
method for aggregating the measurements by computing the 75th ments provide a clinically meaningful assessment of PD severity.
percentile gait speed in each aggregation window. Such aggregation Figure 3C shows that the two common standards for assessing
method focuses on high-speed gait measurements, and hence better re- PD severity, namely, the MDS-UPDRS and Hoehn and Yahr (H&Y)
flects performance during ON times, defined as periods of improved stage (21), correlated strongly with in-home gait speed measure-
mobility in response to levodopa. The results are similar; specifically, ments but had a weak correlation with in-clinic measurements of
the 75th percentile gait speed and the associated CI cross the 95% Timed Up and Go (TUG) (22) and the Ten Meter Walk Test
threshold (n = 50) with a window size of 14 days. Overall, our anal- (TMWT). This result is consistent with past work, which shows
ysis shows that aggregating gait measurements over 2 weeks or longer weak correlation between in-clinic gait measures and MDS-UPDRS
leads to robust and repeatable results. (11, 23–25). The reason might be because gait speed measured in
Liu et al., Sci. Transl. Med. 14, eadc9669 (2022) 21 September 2022 3 of 13
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A 1.1 C
1.0 r = –0.83
Timed Up and Go
subscore
MDS-UPDRS
MDS-UPDRS
total score
0.8
stage
0.7
part
0.6
1.00 –0.86 –0.83 –0.70 –0.33 0.40
In-home gait speed (<0.001) (<0.001) (<0.001) (<0.001) (0.020) (<0.01)
0.5
0 20 40 60 80 100
MDS-UPDRS total score MDS-UPDRS –0.86 1.00 0.92 0.80 0.33 –0.40
part sub-score (<0.001) (<0.001) (<0.001) (<0.001) (0.018) (<0.01)
B 1.1
MDS-UPDRS –0.83 0.92 1.00 0.83 0.41 –0.41
r = –0.86
1.0 P < 0.001 total score (<0.001) (<0.001) (<0.001) (<0.001) (<0.01) (<0.01)
In-home gait speed (m/s)
0.6
0.40 –0.40 –0.41 –0.33 –0.70 1.00
Ten Meter Walk Test (<0.01) (<0.01) (<0.01) (0.018) (<0.001) (<0.001)
0.5
0 10 20 30 40 50
MDS-UPDRS part subscore
Fig. 3. Correlation between in-home gait speed and standard PD outcome measures. (A) and (B) plot the 75th percentile gait speed (from the 14 days following the
baseline visit) against the MDS-UPDRS ON state at baseline. (C) Pairwise Pearson correlation between in-home gait speed, MDS-UPDRS part III subscore, MDS-UPDRS total
score, H&Y, TUG, and TMWT (n = 50).
daily home activities reflects the habitual gait performance (26, 27) other differences between the two individuals. Thus, we used linear
and is less likely to be confounded by observer or Hawthorne effects mixed-effects models to analyze the rate of gait decline among the
(28). To further understand the relation between in-home and in-clinic PD cohort and the control cohort. The models included random
gait assessment, we compared the TUG and TMWT against the me- effects of slope and intercept for each participant and were adjusted
dian (50th percentile), 75th percentile, and 90th percentile in-home for demographic covariates. There was a significant decline in gait
gait speed (table S2). We found that the correlation between in-home speed over time of −0.026 m/s (95% CI, −0.034 to −0.019; P < 0.001)
gait speed and TUG/TMWT increased with the higher gait percen- per year for participants with PD and −0.015 m/s (95% CI, −0.025
tiles, indicating that in-clinic measurements focus on patient capac- to −0.004; P = 0.007) per year for control participants as shown in
ity, whereas in-home measurements focus on patient performance. Fig. 4B. These results show that older people, with and without PD,
Overall, the results provide evidence of the feasibility of in-home slow down as they age further (19, 29–32). However, individuals with
gait speed as a marker of PD severity. PD slow down much faster than those without PD. In other words,
their gait speed declines almost twice as fast. To evaluate the statis-
In-home gait speed as a marker of PD progression tical significance of the difference in gait speed decline between in-
Next, we investigated whether the decline in gait speed over time dividuals with and without PD, a group and time interaction term
differs between participants with and without PD and whether such was included in the model. We observed a statistically significant
a decline can capture disease progression among those with PD. This interaction between group and time with a greater rate of decline in
analysis is performed on the participants in the longitudinal study. the PD group (P = 0.04). These results confirm previous evidence
To gain insight into how gait speed changes over time, we plot in that changes in gait differ significantly between individuals with and
Fig. 4A the change in gait speed over 1 year for two participants without PD (33), and demonstrate that such difference can be cap-
randomly selected from the PD and control cohorts who completed tured at home using passive and touchless measurements.
12 months of monitoring. Regression analysis shows that the rate of Another important finding is that PD progression was not cap-
decline for the participant with PD was −0.030 m/s per year (95% tured reliably by changes in MDS-UPDRS at baseline, month 6, and
CI, −0.038 to −0.022; P < 0.001), which is faster than the gait de- month 12. We applied a similar linear mixed-effects model to the
cline of the control participant, which was −0.014 m/s per year (95% MDS-UPDRS values. The results show that the 1-year progression
CI, −0.019 to −0.010; P < 0.001). in MDS-UPDRS did not achieve statistical significance (part III sub-
Simply looking at gait decline in the two participants in Fig. 4A, score model, P = 0.67; total score model, P = 0.71). This indicates
one cannot judge whether the difference is due to the disease or that in contrast to in-home gait speed, MDS-UPDRS part III and
Liu et al., Sci. Transl. Med. 14, eadc9669 (2022) 21 September 2022 4 of 13
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A B
0.86 0.64 0.02
A control participant A PD participant
0.01
0.84 0.62
–0.02
0.80 0.58
–0.03
0.78 0.56
–0.04
–0.05
0.76 0.54 0 2 4 6 8 10 12
0 2 4 6 8 10 12 0 2 4 6 8 10 12 Time (month)
Time (month) Time (month)
Control cohort Control 95% CI Control individual
total assessments were unable to deliver sufficiently sensitive markers goal, we exploited the fact that patients usually have regular medi-
of 1-year disease progression in this population. This result is con- cation schedules, and hence, their motor fluctuations repeat around
sistent with past work that reported that the 1-year progression the same time across different days. Thus, for participants who were
in MDS-UPDRS part III was not statistically significant even with taking levodopa, we computed the intraday gait speed, which we de-
a population of over 200 individuals with PD (31). Table S7 fine as the gait speed of an individual as a function of the hour in the day.
shows that the lack of statistical significance can persist even in We compared the intraday gait speed of each participant with their
larger populations. ON-OFF states through the day, as reported in their Hauser diaries.
Last, to control for the effects caused by changes in symptomatic Figure 5 shows evidence that in-home gait speed can capture
therapy, we repeated the above analysis only for intervals without medication response and motor fluctuations. In particular, Fig. 5A
any changes in therapy. The resulting 1-year gait decline was −0.028 m/s plots the intraday gait speed of four participants with PD, along with
(95% CI, −0.037 to −0.018; P < 0.001) and was significantly higher the percentage of ON time, as reported in their Hauser diaries. The
than the control group (P < 0.034). We also applied the same statis- top graphs reveal that in-home gait speed oscillates in response to
tical analysis to the MDS-UPDRS total score and part III subscore, medication administration. One possible explanation for these oscilla-
for the same participants over the same period. The progression in tions is that they reflect the effect of medications in only controlling
MDS-UPDRS remained statistically not significant (P = 0.82 for the symptoms; thus, when the patient takes their medications, their
total score and P = 0.49 for part III subscore). Overall, the analysis gait speed improves, but within 1 to 2 hours, the medication impact
above shows that in-home gait speed might be a sensitive marker of wears off and the gait speed declines again, until the patient takes
PD progression. the next dose. The figure also shows that the degree to which the
oscillations are controlled differs across patients. For example, PD1’s
Gait speed as a marker of PD motor fluctuation motor symptoms are relatively well controlled; this is apparent in
and medication response PD1’s intraday gait speed, which is fairly stable throughout the day
Within 3 to 5 years of levodopa treatment, about 50% of individuals and night, and is confirmed in his Hauser diary, which reports no
with PD begin to develop motor fluctuations (34), characterized by a OFF time (compare that to PD2, PD3, and PD4, who experience
decline in the duration of benefit of each dose with emergent motor a large difference between day-time and night-time gait speed and
fluctuations, a phenomenon known as “wearing-off” or “ON-OFF” wide fluctuations in their gait speed throughout the day). Also, note
effect (3). Now, clinicians and researchers may assess such ON-OFF that the fluctuations are aligned with the medication times and the
symptoms using the Hauser diary (35), in which patients self-report percentage of ON time in their Hauser diaries.
the time they take their medications, and their functional status In addition, we found that changes in intraday gait speed profiles
every 30 min as ON or OFF (35). Filling in the Hauser diary impos- reflected adjustments in medication plan. Figure 5B depicts the in-
es a burden on participants and often results in low reliability due to traday gait speed of a participant with PD before and after his med-
poor adherence and recall bias (36, 37). ication adjustment. Before the medication adjustment, the patient’s
We examined the ability of our system to capture medication motor performance fluctuated widely throughout the day, showing
impact on motor fluctuations and ON-OFF symptoms. Toward this clear peaks and valleys. After reducing the dose and increasing the
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1: Ropinirole 8 mg ER × 1 + Rasagiline 1 1–3: Pramipexole 0.75 mg × 1 + 1–3: C/L 25/100 mg × 1 1–5: C/L 25/100 mg × 1.5
mg × 1 + Amantadine 100 mg × 1 carbidopa/levodopa (C/L) 25–100 mg × 2
2: Amantadine 100 mg × 1
3: Ropinirole 8 mg ER × 1 45–55th 40–60th
Median ON OFF SLEEP
percentile percentile
B C
1.0
C/L 25/100 mg 2 tab 0.10 n=2
3 times a day
0.9
Gait speed (m/s)
r = 0.74 n=6
P < 0.001 n=1
0.8 0.09
0.7
0.08
0.6 Medication wears off
Variance of gait speed
0.07
0.5
4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 0 1 2 3
Hour in the day n=9
1.0 0.06
C/L 25/100 mg 1 tab
6 times a day
0.9
Gait speed (m/s)
n = 16
0.05
0.8
0.7 0.04
Reduced motor fluctuation
0.6
0.03
0.5
4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 0 1 2 3
Hour in the day 0.02
40–60th percentile Median gait speed Normal Slight Mild Moderate Severe
Fig. 5. Intra-day gait speed capture of motor fluctuations, adjustments in medication plans, and self-reported disease impact on daily function. (A) Top
figures: Intraday gait speed distribution of four participants with PD measured using 2 months of data. The dashed black lines refer to the medication schedule.
Bottom figures: Normalized histograms of ON-OFF status of the participants in the top figures, over the same period, as reported in the participants’ Hauser diaries.
(B) Intraday gait speed profile of a participant with PD who experienced a medication adjustment. Top plot: Profile from the period following the baseline visit when
the participant took two tablets of carbidopa/levodopa (25/100 mg three times per day). Bottom plot: Profile from the period following the month 6 visit when his
medication dose was adjusted to one tablet six times per day, showing reduced motor fluctuation. (C) Relationship between intraday gait speed fluctuations and
self-reported disease impact on daily function, which is taken from the MDS-UPDRS functional impact of fluctuation subscore (n = 34). The figure also reports the
Spearman’s rank-order correlation.
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A 12 50
B
0.8
P = 0.03 P < 0.01 Decline before
11 hospitalization After being back
40
Time in bed per day (hour)
30
9 In hospital
0.6
8 20
11 days
7 0.5 //
–14 –12 –10 –8 –6 –4 –2 0 12 14 16 18 20 22 24 26 28
10
6 Day w.r.t. hospitalization
Fig. 6. System-derived measurements reflecting symptom changes due to COVID-19 lockdown and hospitalization. (A) Changes in time in bed per day and num-
ber of walks per day before and after COVID-19 lockdown measurements (n = 17). (B) Longitudinal in-home gait speed trajectory of a participant with PD before and after
his hospitalization. This individual is a 75-year-old man with PD (baseline MDS-UPDRS part III/total score = 33/54) who was hospitalized for 11 days due to newly discov-
ered atrial fibrillation.
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assessing gait speed in the real-world environment is further demon- evaluation of the system is limited by the precision of standard
strated by our data, which show that comprehensive clinical tests PD ratings and patients’ self-reported outcomes. In particular, the
such as the MDS-UPDRS correlate strongly with in-home gait MDS-UPDRS ratings were acquired through episodic in-clinic as-
speed but correlate only weakly with in-clinic measures of gait sessments and could be affected by patients’ physical status on the
speed. These results are aligned with past observations that MDS- day of in-clinic visit. Fourth, gait speed is a general metric not spe-
UPDRS total and part III scores are weakly correlated with in-clinic cific to PD and could be affected by other health issues. Our covari-
measures of gait speed (11, 23–25). Our results also show that ate analysis, however, provides evidence that none of the common
in-clinic gait measures such as TUG and TMWT correlate better comorbidities constitutes a confounding factor for our results. Last,
with the faster instances of in-home gait speed, which is consistent PD exhibits several gait impairments that are not studied in this
with past reports (41) that in-clinic gait captures patient capacity, paper. Some impairments such as falls and freezing can potentially
whereas in-home gait captures patient performance. This indicates be captured by our radio device (47, 48) and provide a natural topic
that in-home and in-clinic gait measurements can play a comple- for future work. Despite the above limitations, we believe that the
mentary role in PD assessment. study provides important insights and addresses key unmet needs
The results in this study might have important implications for in clinical care and drug development in PD.
clinical trials and the development of better and possibly personal- Our work is aligned with recent interest in leveraging digital
ized therapies for treating PD. A key challenge for PD clinical trials technologies for assessing PD. Technologies that use cellphones or
stems from the fact that the disease evolves slowly, yet MDS-UPDRS is wearable devices are widely available and can be used inside and out-
not sufficiently sensitive to small changes in symptoms. As a result, side the home. However, they require patients to wear and charge
PD clinical trials need to last for multiple years and enroll hundreds devices (11, 41, 49–52), and unless the movements are scripted
of participants before differences in MDS-UPDRS can be reported (11, 49), their correlation with the MDS-UPDRS is inferior to our
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this article, we consider only data from the first year of monitoring. methods that identify people using the radio signals that bounce off
All participants with PD were screened and met the UK PD Society their bodies (68–70). In this paper, we leverage the method developed
Brain Bank Clinical Diagnostic Criteria; control individuals had no by Hsu et al. (67). Specifically, the device uses standard signal pro-
evidence of primary or secondary Parkinsonism. After enrollment cessing techniques such as Frequency-Modulated Continuous-Wave
and screening, a study coordinator installed the wireless device in (FMCW) and antenna arrays to zoom in on radio signals from each
the participant’s home and connected the device to the patient’s voxel in space and separate signals based on spatial locations. To
home Wi-Fi network. Study coordinators also created a basic floor identify signals from the participant from others, participants are
map of the monitored area to allow post hoc assessment of partici- asked to wear a coin-size accelerometer for the first 2 weeks of the
pant position in the home. study. The accelerometer data are then used to train a machine
Enrolled participants underwent clinical assessments at baseline, learning classifier that identifies the radio signals that bounce off
and in the longitudinal study, participants have visits at 6 months, the participant from signals that bounce off other people and objects
12 months, and 2 years after installation. During these visits, a move- in the house. Once the classifier is trained, participants do not need
ment disorder specialist conducted PD assessments including the to wear the accelerometer and can be identified solely from radio
MDS-UPDRS parts I to IV, H&Y stage, and TUG, among others. signals using the aforementioned classifier. As shown by Hsu et al.
The longitudinal study was started before and has continued during (67), this method is accurate and its average identification accuracy
the COVID-19 pandemic, resulting in a shift in clinical assessments, across different homes and individuals is 90%.
with some visits being conducted remotely. However, all baseline vis- The same radio device was used to detect errors in medication
its were conducted in person. During remote visits, measures that self-administration (71) and monitor patients with Alzheimer’s dis-
require in-person assessment, including TUG and TMWT, were not ease (72), endometriosis (73), COVID-19 (74), and facioscapulohu-
performed. The feasibility of remote performance of the MDS-UPDRS meral muscular dystrophy (FSHD) (75). Also, we have explored the
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We assessed the correlation between in-home gait speed and SPD ij − SPD baseline,i = u 0i + ( 1 + u 1i) × T ij + ij + ∑ v × v
clinical PD outcome measures [MDS-UPDRS part III subscore and
total score (7), H&Y stage (21), TUG (22), and TMWT] at the base- where u0 ∼ Normal(0, u0), u1 ∼ Normal(0, u1), ∼ Normal(0, ).
line visit using Pearson correlation. Baseline in-home gait speed Notably, we did not include a fixed-effect intercept in the model
was measured from the first 14 days after the baseline visit. We used because we expect no gait speed decline at baseline.
the 75th percentile in-home gait speed to reflect gait speed during For combined PD and control cohort analysis, we included the
ON time. These clinical PD outcomes were measured when partici- group × time interaction term in the formula
pants were on medication.
Analysis of confounding factors SPD ij − SPD baseline,i = u 0i + ( 1 + u 1i) × T ij+
We have performed statistical analyses to ensure that the correla- ij + 2 × cohort ij × T ij + ∑ v × v
tion between in-home gait speed and the MDS-UPDRS (total
and part III scores) is not affected by confounding factors. In addi- where u0 ∼ Normal(0, u0), u1 ∼ Normal(0, u1), ∼ Normal(0, ).
tion to demographics (age, gender, ethnicity, race, and education), Restricted maximum likelihood estimation was used for all models
we consider the following 15 comorbidities: cognitive performance; to estimate the parameters.
overall health; cardiac health; hypertension; vascular health; Insights into various events at home
respiratory system health; eye, ear, nose, and throat (EENT) As an exploratory endpoint, we collected from each participant in-
health; upper gastrointestinal (GI) health; lower gastrointestinal formation on events of interest during the monitoring period, in-
health; hepatic health; renal health; other genitourinary (GU) health; cluding societal events, such as local lockdowns in the setting of the
musculoskeletal and integumentary health; endocrine and metabolic COVID-19 pandemic, and personal medical events, such as hospi-
health; and psychiatric and behavioral health. We score cognitive talizations and medication adjustment. We assessed the impact of
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responsibility of the authors and does not necessarily represent the official views of the NIH. received honoraria for speaking at American Academy of Neurology, American Neurological
Funding: The work was supported by a grant from the NIH (P50NS108676) to Y.L., G.Z., C.G.T., Association, Excellus BlueCross BlueShield, International Parkinson’s and Movement Disorders
S.J.-R., E.M.W., T.L.M., M.E.P., J.M.S., R.M.W., Y.Y., T.N., K.J.L., J.L.A., R.B.S., K.K., T.E., E.R.D., and D.K. Society, National Multiple Sclerosis Society, Northwestern University, Physicians Education
and by a grant from the Michael J. Fox Foundation (15069) to R.H. Author contributions: Resource, LLC, Stanford University, Texas Neurological Society, and Weill Cornell;
Conceptualization: Y.L., G.Z., C.G.T., T.E., E.R.D., and D.K. Methodology: Y.L., G.Z., and compensation for consulting services from Abbott, Abbvie, Acadia, Acorda, Alzheimer’s Drug
D.K. Software (data collection/visualization, machine learning, and signal processing): Y.L. and Discovery Foundation, Ascension Health Alliance, Bial-Biotech Investments Inc., Biogen,
R.H. Software (statistical analysis and validation): Y.L. and G.Z. Validation: Y.L., G.Z., R.H., and BluePrint Orphan, California Pacific Medical Center, Caraway Therapeutics, Clintrex, Curasen
D.K. Formal analysis: Y.L., G.Z., and D.K. Investigation: Y.L. G.Z., C.G.T., R.H., S.J.-R., E.M.W., T.L.M., Therapeutics, DeciBio, Denali Therapeutics, Eli Lilly, Grand Rounds, and Huntington Study
M.E.P., J.M.S., R.M.W., T.N., K.J.L., J.L.A., R.B.S., K.K., and T.E. Resources: Y.L., G.Z., C.G.T., R.H., Group, medical-legal services, Mediflix, Medopad, Medrhythms, Michael J. Fox Foundation,
S.J.-R., E.M.W., T.L.M., M.E.P., J.M.S., R.M.W., T.N., T.E., E.R.D., and D.K. Data curation: Y.L., G.Z., MJH Holding LLC, NACCME, Neurocrine, NeuroDerm, Olson Research Group, Origent Data
C.G.T., R.H., S.J.-R., E.M.W., T.L.M., M.E.P., J.M.S., R.M.W., Y.Y., and T.N. Writing—original draft: Sciences, Otsuka, Pear Therapeutic, Praxis, Prilenia, Roche, Sanofi, Seminal Healthcare, Spark,
Y.L., G.Z., C.G.T., and D.K. Writing—review and editing: Y.L., G.Z., C.G.T., R.H., J.L.A., K.J.L., R.B.S., Springer Healthcare, Sunovion Pharma, Sutter Bay Hospitals, Theravance, University of
K.K., T.E., E.R.D., and D.K. Visualization: Y.L. and G.Z. Supervision: T.E., E.R.D., and D.K. Project California Irvine, and WebMD; research support from Abbvie, Acadia Pharmaceuticals, Biogen,
administration: S.J.-R., E.M.W., M.E.P., R.M.W., T.E., E.R.D., and D.K. Funding acquisition: E.R.D. Biosensics, Burroughs Wellcome Fund, CuraSen, Greater Rochester Health Foundation,
and D.K. Competing interests: T.N. has received research support from the NIH and the Huntington Study Group, Michael J. Fox Foundation, NIH, Patient-Centered Outcomes
Michael J. Fox Foundation. K.J.L. has research support from the NIH/NINDS, Acadia, AbbVie, Research Institute, Pfizer, PhotoPharmics, Safra Foundation, and Wave Life Sciences; editorial
and Genentech. J.L.A. has received honoraria for speaking at the Huntington Study Group and services for Karger Publications; and ownership interests with Grand Rounds (second opinion
American Neurological Association; compensation for consulting services from VisualDx and service). D.K. and R.H. are cofounders of Emerald Innovations. D.K. receives research funding
the Huntington Study Group; and research support from Biogen, Michael J. Fox Foundation, from the NIH and Michael J. Fox Foundation and serves on the scientific advisory board of
and NIH/NINDS. R.B.S. has received compensation for consulting services from Parkinson’s Janssen and the data science advisory board of Amgen. The remaining authors declare that
Foundation, Voyager Therapeutics, and Escape Bio and research support from the NIH, they have no competing interests. Data and materials availability: All data associated with
Michael J. Fox Foundation for Parkinson’s Research, Biohaven Pharmaceuticals, Acadia this study are present in the paper or the Supplementary Materials. The code is publicly
Pharmaceuticals, and Parkinson Study Group. K.K. has received compensation for consulting available from the project’s website (https://rf-pd-gait.csail.mit.edu) or GitHub (https://github.
services from Clintrex Research Corp., Roche/Genentech, and Novartis; research support from com/firstmover/rf-pd-gait). Additional data are available by request, subject to signing a data
the NIH (NINDS, NCATS) and Michael J Fox Foundation; and ownership interests with Clintrex
Liu et al., Sci. Transl. Med. 14, eadc9669 (2022) 21 September 2022 13 of 13
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